Current research in physiology最新文献_第4页

Sex differences in the association between albuminuria and vascular health in individuals living with chronic kidney disease 慢性肾脏疾病患者蛋白尿与血管健康相关性的性别差异

IF 2.1 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100145

Badal S.B. Pattar , Sofia B. Ahmed , Jessalyn K. Holodinsky , Nicole Larsen , Sakshi Kharbanda , Sarah Rabi , Victoria Riehl-Tonn , Darlene Y. Sola , Sarah Blayney , Sandra M. Dumanski

Cardiovascular disease is the leading cause of death in chronic kidney disease (CKD). Albuminuria, a marker of CKD severity, is independently associated with cardiovascular disease, however limited studies explore the impact of sex. We aimed to explore sex differences in the association between albuminuria and vascular health in individuals living with CKD. Albuminuria was quantified through urine albumin-to-creatinine ratio (uACR) and measures of vascular health included Aortic Augmentation Index (AIx), Pulse Wave Velocity (PWV) and Mean Arterial Pressure (MAP). Multivariable linear regression analyses estimated the association between uACR and each outcome, and sex was assessed as an effect modifier. Adults living with CKD were recruited from nephrology clinics in Calgary, Canada and 66 participants (39 female, 27 male) were included in this study. A higher eGFR (89[56] versus 58[50] ml/min/1.73m2) and lower uACR (32[405] versus 386[933] mg/g) were observed in females. Sex modified the relationship between uACR and AIx; with a positive association in females (

β

= 0.02; p < 0.01), and no relationship in males (

β

= -0.004; p = 0.16). Positive relationships between uACR and both PWV and MAP were observed, though sex did not modify either relationship. Further research to elucidate the mechanisms underpinning these sex differences are necessary to optimize and personalize cardiovascular risk reduction strategies in CKD.

心血管疾病是导致慢性肾脏疾病（CKD）死亡的主要原因。蛋白尿是CKD严重程度的一个标志，与心血管疾病独立相关，但探讨性别影响的研究有限。我们旨在探讨慢性肾病患者蛋白尿与血管健康之间关系的性别差异。通过尿白蛋白与肌酐比值（uACR）量化尿白蛋白，血管健康指标包括主动脉增强指数（AIx）、脉搏波速度（PWV）和平均动脉压（MAP）。多变量线性回归分析估计了uACR与每个结果之间的关联，性别被评估为影响修饰因子。研究人员从加拿大卡尔加里的肾脏科诊所招募了66名患有慢性肾病的成年人（39名女性，27名男性）。在女性中观察到较高的eGFR（89[50]对58[50]ml/min/1.73m2）和较低的uACR（32[405]对386[933]mg/g）。性别改变了uACR与AIx之间的关系；与女性呈正相关(β = 0.02；p & lt;0.01)，男性无相关性(β = -0.004；p = 0.16)。uACR与PWV和MAP之间存在正相关关系，但性别不影响这两种关系。进一步研究这些性别差异背后的机制对于优化和个性化CKD心血管风险降低策略是必要的。

{"title":"Sex differences in the association between albuminuria and vascular health in individuals living with chronic kidney disease","authors":"Badal S.B. Pattar , Sofia B. Ahmed , Jessalyn K. Holodinsky , Nicole Larsen , Sakshi Kharbanda , Sarah Rabi , Victoria Riehl-Tonn , Darlene Y. Sola , Sarah Blayney , Sandra M. Dumanski","doi":"10.1016/j.crphys.2025.100145","DOIUrl":"10.1016/j.crphys.2025.100145","url":null,"abstract":"<div><div>Cardiovascular disease is the leading cause of death in chronic kidney disease (CKD). Albuminuria, a marker of CKD severity, is independently associated with cardiovascular disease, however limited studies explore the impact of sex. We aimed to explore sex differences in the association between albuminuria and vascular health in individuals living with CKD. Albuminuria was quantified through urine albumin-to-creatinine ratio (uACR) and measures of vascular health included Aortic Augmentation Index (AIx), Pulse Wave Velocity (PWV) and Mean Arterial Pressure (MAP). Multivariable linear regression analyses estimated the association between uACR and each outcome, and sex was assessed as an effect modifier. Adults living with CKD were recruited from nephrology clinics in Calgary, Canada and 66 participants (39 female, 27 male) were included in this study. A higher eGFR (89[56] versus 58[50] ml/min/1.73m2) and lower uACR (32[405] versus 386[933] mg/g) were observed in females. Sex modified the relationship between uACR and AIx; with a positive association in females (<span><math><mrow><mi>β</mi></mrow></math></span> = 0.02; p < 0.01), and no relationship in males (<span><math><mrow><mi>β</mi></mrow></math></span> = -0.004; p = 0.16). Positive relationships between uACR and both PWV and MAP were observed, though sex did not modify either relationship. Further research to elucidate the mechanisms underpinning these sex differences are necessary to optimize and personalize cardiovascular risk reduction strategies in CKD.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100145"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143924663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High-intensity training and irisin response: A possible molecular cross-talk for irisin response 高强度训练和鸢尾素反应：鸢尾素反应可能的分子串扰

IF 1.7 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100163

Ping Li , Ligang Tong , Xuecui Bi

Physical exercise is widely recognized for its positive effect on health through alterations in genetic, molecular, or tissue-level pleiotropic effects. The extent of these advantages hinges on the intensity that elicits optimal threshold adaptation, facilitating interactions and communication within or between the cells. This requires the activation of several proteins, enzymes, and hormones. Irisin, an exercise-triggered hormone, is pivotal in converting white fat into brown fat, enhancing bone health, and optimizing brain functions. The activation of irisin is contingent upon precise exercise protocols that trigger several molecular cross-talks. However, no specific exercise protocols (types/intensity/duration) have been developed. Therefore, establishing specific exercise protocols could reveal irisin-induced benefits on bone and brain health. The present review discussed how high-intensity training (HIT) triggers the irisin response by activating its upstream and downstream molecular signaling pathways and how HIT helps to cross-talk these signaling pathways to improve irisin response.

体育锻炼因其通过改变基因、分子或组织水平的多效效应而对健康产生积极影响而被广泛认可。这些优势的程度取决于引发最佳阈值适应的强度，促进细胞内或细胞间的相互作用和交流。这需要激活几种蛋白质、酶和激素。鸢尾素是一种运动触发的激素，在将白色脂肪转化为棕色脂肪、增强骨骼健康和优化大脑功能方面起着关键作用。鸢尾素的激活取决于触发几个分子交叉对话的精确运动方案。然而，没有制定具体的运动方案（类型/强度/持续时间）。因此，建立特定的运动方案可以揭示鸢尾素对骨骼和大脑健康的益处。本文综述了高强度训练（HIT）如何通过激活鸢尾素的上下游分子信号通路来触发鸢尾素反应，以及HIT如何帮助这些信号通路串扰以改善鸢尾素反应。

引用次数: 0

Acidosis enhances contribution of Ca2+-activated chloride channels to vascular tone regulation in early postnatal period 酸中毒增强Ca2+激活的氯离子通道对产后早期血管张力调节的贡献

IF 2.1 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100143

Anastasia A. Shvetsova , Margarita A. Khlystova , Valentina S. Shateeva , Sofia D. Simonenko , Anna A. Borzykh , Denis V. Abramochkin , Dina K. Gaynullina

Introduction

Acidosis often occurs during clinical complications in newborns and can lead to changes in the mechanisms of arterial tone regulation. However, it is unknown how acidosis affects the activity of Ca²⁺-activated chloride channels (CaCC) in arteries during early ontogenesis. We hypothesized that their activity may increase during acidosis.

Methods

We studied isometric contractions of saphenous arteries isolated from adult and 10-13-day-old rats. Intracellular pH was measured using a fluorescent indicator BCECF-AM simultaneously with recording the contractile activity of the arterial preparation in isometric mode.

Results

Metabolic acidosis with pH = 6.8 caused a significant decrease in the arterial contractile responses of adult and 10-13-day-old rats. The functional contribution of CaCC was absent in the adult rat arteries both at pH = 7.4 and pH = 6.8. However, in 10-13-day-old rat pups, the functional contribution of CaCC was higher at pH = 6.8 compared to pH = 7.4.

Conclusion

Acidosis augments the functional role of CaCC in arteries during early postnatal ontogenesis, but not in adulthood.

酸中毒常发生在新生儿临床并发症中，可导致动脉张力调节机制的改变。然而，目前尚不清楚酸中毒如何影响早期个体形成过程中动脉中Ca2+激活的氯离子通道（CaCC）的活性。我们假设它们的活性可能在酸中毒期间增加。方法观察成年大鼠和10-13日龄大鼠隐动脉的等长收缩。使用荧光指示剂BCECF-AM测量细胞内pH值，同时以等长模式记录动脉制剂的收缩活性。结果pH = 6.8的代谢性酸中毒使成年大鼠和10-13日龄大鼠的动脉收缩反应明显降低。在pH = 7.4和pH = 6.8时，成年大鼠动脉中没有CaCC的功能贡献。然而，在10-13日龄的大鼠幼崽中，pH = 6.8时CaCC的功能贡献高于pH = 7.4。结论在出生后早期个体发育过程中，酸中毒增强了CaCC在动脉中的功能作用，但在成年期没有。

{"title":"Acidosis enhances contribution of Ca2+-activated chloride channels to vascular tone regulation in early postnatal period","authors":"Anastasia A. Shvetsova , Margarita A. Khlystova , Valentina S. Shateeva , Sofia D. Simonenko , Anna A. Borzykh , Denis V. Abramochkin , Dina K. Gaynullina","doi":"10.1016/j.crphys.2025.100143","DOIUrl":"10.1016/j.crphys.2025.100143","url":null,"abstract":"<div><h3>Introduction</h3><div>Acidosis often occurs during clinical complications in newborns and can lead to changes in the mechanisms of arterial tone regulation. However, it is unknown how acidosis affects the activity of Ca<sup>2+</sup>-activated chloride channels (CaCC) in arteries during early ontogenesis. We hypothesized that their activity may increase during acidosis.</div></div><div><h3>Methods</h3><div>We studied isometric contractions of saphenous arteries isolated from adult and 10-13-day-old rats. Intracellular pH was measured using a fluorescent indicator BCECF-AM simultaneously with recording the contractile activity of the arterial preparation in isometric mode.</div></div><div><h3>Results</h3><div>Metabolic acidosis with pH = 6.8 caused a significant decrease in the arterial contractile responses of adult and 10-13-day-old rats. The functional contribution of CaCC was absent in the adult rat arteries both at pH = 7.4 and pH = 6.8. However, in 10-13-day-old rat pups, the functional contribution of CaCC was higher at pH = 6.8 compared to pH = 7.4.</div></div><div><h3>Conclusion</h3><div>Acidosis augments the functional role of CaCC in arteries during early postnatal ontogenesis, but not in adulthood.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100143"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice 野生型和GIRK2突变小鼠注射吗啡后延髓腹侧呼吸控制中心1H mrs代谢物的变化

IF 2.1 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100147

Ozra Dehkordi , Stephen Lin , Safia Mohamud , Richard M. Millis , Paul C. Wang

Respiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain poorly understood. G-protein-gated inwardly rectifying potassium (GIRK) channels, especially the GIRK2 subunit, are expressed in rhythm-generating neurons of the pre-Bötzinger complex and have been implicated in opioid-induced respiratory depression. Nonetheless, their specific role in morphine-induced neurochemical changes is not yet fully defined. In this study, in vivo proton magnetic resonance spectroscopy (¹H MRS) was used in mice to assess morphine-induced metabolite changes in ventral brainstem regions encompassing the pre-Bötzinger complex. Wild-type mice were compared with GIRK2 heterozygous (GIRK2⁺/⁻) mutants. Baseline levels of several metabolites including glutamate (Glu), myo-inositol (Ins), N-acetylaspartate plus N-acetylaspartylglutamate (NAA + NAAG), and glutamate plus glutamine (Glu + Gln) differed significantly between GIRK2⁺/⁻ and wild-type mice. Despite these baseline differences, many of morphine's effects on metabolite levels were similar in the wild-type and GIRK2⁺/⁻ mice. Morphine increased phosphocreatine (PCr) in both genotypes, while total creatine (Cr + PCr) decreased only in the wild-type mice. Glutamine levels increased significantly in both groups. Notably, NAA decreased in wild-type but increased in GIRK2⁺/⁻ mice, whereas NAA + NAAG decreased in both. These findings demonstrate that chronic morphine exposure induces substantial neurochemical changes in brainstem respiratory centers. Although the GIRK2⁺/ ^- mutation altered some of the metabolite responses, it does not fully block morphine's effects, highlighting the complexity of opioid-induced adaptations in the respiratory control networks.

呼吸抑制是阿片类药物过量死亡的主要原因，并与反复使用吗啡后产生耐受性密切相关。然而，脑干区域调节呼吸的神经化学适应性，特别是在慢性阿片类药物暴露下，仍然知之甚少。g蛋白门控内向整流钾（GIRK）通道，特别是GIRK2亚基，在pre-Bötzinger复合体的节律生成神经元中表达，并与阿片类药物诱导的呼吸抑制有关。尽管如此，它们在吗啡诱导的神经化学变化中的具体作用尚未完全确定。在这项研究中，在小鼠体内使用质子磁共振波谱（1H MRS）来评估吗啡诱导的包括pre-Bötzinger复合物的腹侧脑干区域代谢物的变化。将野生型小鼠与GIRK2杂合（GIRK2+/−）突变体进行比较。几种代谢物的基线水平，包括谷氨酸（Glu）、肌醇（Ins）、n -乙酰天冬氨酸加n -乙酰天冬氨酸（NAA + NAAG）和谷氨酸加谷氨酰胺（Glu + Gln），在GIRK2+/−和野生型小鼠之间存在显著差异。尽管存在这些基线差异，但吗啡对野生型和GIRK2+/−小鼠代谢物水平的许多影响是相似的。吗啡增加了两种基因型小鼠的磷酸肌酸（PCr），而总肌酸（Cr + PCr）仅在野生型小鼠中降低。两组的谷氨酰胺水平均显著升高。值得注意的是，NAA在野生型小鼠中降低，而在GIRK2+/−小鼠中升高，而NAA + NAAG在两者中均降低。这些发现表明，慢性吗啡暴露会引起脑干呼吸中枢的实质性神经化学变化。尽管GIRK2+/ -突变改变了一些代谢物反应，但它并不能完全阻断吗啡的作用，这突出了阿片类药物诱导的呼吸控制网络适应的复杂性。

{"title":"1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice","authors":"Ozra Dehkordi , Stephen Lin , Safia Mohamud , Richard M. Millis , Paul C. Wang","doi":"10.1016/j.crphys.2025.100147","DOIUrl":"10.1016/j.crphys.2025.100147","url":null,"abstract":"<div><div>Respiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain poorly understood. G-protein-gated inwardly rectifying potassium (GIRK) channels, especially the GIRK2 subunit, are expressed in rhythm-generating neurons of the pre-Bötzinger complex and have been implicated in opioid-induced respiratory depression. Nonetheless, their specific role in morphine-induced neurochemical changes is not yet fully defined. In this study, <em>in vivo</em> proton magnetic resonance spectroscopy (<sup>1</sup>H MRS) was used in mice to assess morphine-induced metabolite changes in ventral brainstem regions encompassing the pre-Bötzinger complex. Wild-type mice were compared with GIRK2 heterozygous (GIRK2<sup>+</sup>/<sup>−</sup>) mutants. Baseline levels of several metabolites including glutamate (Glu), myo-inositol (Ins), N-acetylaspartate plus N-acetylaspartylglutamate (NAA + NAAG), and glutamate plus glutamine (Glu + Gln) differed significantly between GIRK2<sup>+</sup>/<sup>−</sup> and wild-type mice. Despite these baseline differences, many of morphine's effects on metabolite levels were similar in the wild-type and GIRK2<sup>+</sup>/<sup>−</sup> mice. Morphine increased phosphocreatine (PCr) in both genotypes, while total creatine (Cr + PCr) decreased only in the wild-type mice. Glutamine levels increased significantly in both groups. Notably, NAA decreased in wild-type but increased in GIRK2<sup>+</sup>/<sup>−</sup> mice, whereas NAA + NAAG decreased in both. These findings demonstrate that chronic morphine exposure induces substantial neurochemical changes in brainstem respiratory centers. Although the GIRK2<sup>+</sup>/ <sup>-</sup> mutation altered some of the metabolite responses, it does not fully block morphine's effects, highlighting the complexity of opioid-induced adaptations in the respiratory control networks.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100147"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sex and dose differences in morphine administration on renal function, inflammatory and apoptotic markers in male and female Wistar rats 吗啡给药对雌雄Wistar大鼠肾功能、炎症和凋亡标志物的性别和剂量差异

IF 1.7 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100162

Olaoluwa Sesan Olukiran , Oluwadare Joshua Ogundipe , Stephen Taiye Adelodun , Moses Agbomhere Hamed , Olayemi Sola Babatunde , Oluwole Ojo Alese , Rufus Ojo Akomolafe

This study examined the impact of morphine on renal function, antioxidant enzymes, and inflammatory and apoptotic markers in male and female Wistar rats, considering both sex- and dose-dependent effects. 40 Wistar rats (20 male, 20 female), each weighing 120–150 g were used in this study. The control group received distilled water (0.5 mL/100 g b.w), while experimental groups were given morphine orally at 20, 40 and 60 mg/kg daily for 30 days. Renal function, inflammatory, and apoptotic markers were assessed in the plasma and tissue homogenate. Kidneys were preserved in 10 % formo-saline for histological examination. Morphine significantly increased plasma creatinine in both male and female rats, with the increase being more pronounced in males. Caspase-3 and TNF-α were also elevated in both sexes, but with no significant difference between males and females. Male rats showed significantly higher catalase activity and elevated plasma sodium, potassium, phosphate, and chloride ion concentrations compared to females. Photomicrographs revealed that low and medium doses of morphine caused more severe kidney damage in both male and female rats, leading to atrophied glomeruli, widened Bowman's space, and loss of brush border in the tubules. Conversely, high-dose resulted in less pronounced damage, with only a few atrophied glomeruli and indistinct tubules. Morphine induced more pronounced lipid peroxidation and oxidative stress in female rats compared to males, as indicated by changes in their plasma electrolytes and antioxidant enzyme activities. Interestingly, lower dose caused more significant alterations in renal function, oxidative stress and apoptotic markers compared to medium and high doses.

本研究考察了吗啡对雄性和雌性Wistar大鼠肾功能、抗氧化酶、炎症和凋亡标志物的影响，并考虑了性别和剂量依赖效应。Wistar大鼠40只，公20只，母20只，每只体重120 ~ 150 g。对照组给予蒸馏水0.5 mL/100 g b.w，实验组给予吗啡20、40、60 mg/kg，每日口服，连用30 d。在血浆和组织匀浆中评估肾功能、炎症和凋亡标志物。肾脏保存在10%福尔摩生理盐水中进行组织学检查。吗啡显著增加了雄性和雌性大鼠的血浆肌酐，其中雄性的增加更为明显。Caspase-3和TNF-α在两性中均升高，但男女之间无显著差异。雄性大鼠的过氧化氢酶活性明显高于雌性，血浆钠、钾、磷酸盐和氯离子浓度也明显高于雌性大鼠。显微照片显示，低剂量和中剂量吗啡对雄性和雌性大鼠的肾损害更严重，导致肾小球萎缩，鲍曼间隙变宽，小管刷状边界丧失。相反，高剂量导致的损害不那么明显，只有少数肾小球萎缩和小管模糊。吗啡在雌性大鼠中引起的脂质过氧化和氧化应激比雄性大鼠更明显，这可以从它们的血浆电解质和抗氧化酶活性的变化中看出。有趣的是，与中剂量和高剂量相比，低剂量引起的肾功能、氧化应激和凋亡标志物的改变更显著。

{"title":"Sex and dose differences in morphine administration on renal function, inflammatory and apoptotic markers in male and female Wistar rats","authors":"Olaoluwa Sesan Olukiran , Oluwadare Joshua Ogundipe , Stephen Taiye Adelodun , Moses Agbomhere Hamed , Olayemi Sola Babatunde , Oluwole Ojo Alese , Rufus Ojo Akomolafe","doi":"10.1016/j.crphys.2025.100162","DOIUrl":"10.1016/j.crphys.2025.100162","url":null,"abstract":"<div><div>This study examined the impact of morphine on renal function, antioxidant enzymes, and inflammatory and apoptotic markers in male and female Wistar rats, considering both sex- and dose-dependent effects. 40 Wistar rats (20 male, 20 female), each weighing 120–150 g were used in this study. The control group received distilled water (0.5 mL/100 g b.w), while experimental groups were given morphine orally at 20, 40 and 60 mg/kg daily for 30 days. Renal function, inflammatory, and apoptotic markers were assessed in the plasma and tissue homogenate. Kidneys were preserved in 10 % formo-saline for histological examination. Morphine significantly increased plasma creatinine in both male and female rats, with the increase being more pronounced in males. Caspase-3 and TNF-α were also elevated in both sexes, but with no significant difference between males and females. Male rats showed significantly higher catalase activity and elevated plasma sodium, potassium, phosphate, and chloride ion concentrations compared to females. Photomicrographs revealed that low and medium doses of morphine caused more severe kidney damage in both male and female rats, leading to atrophied glomeruli, widened Bowman's space, and loss of brush border in the tubules. Conversely, high-dose resulted in less pronounced damage, with only a few atrophied glomeruli and indistinct tubules. Morphine induced more pronounced lipid peroxidation and oxidative stress in female rats compared to males, as indicated by changes in their plasma electrolytes and antioxidant enzyme activities. Interestingly, lower dose caused more significant alterations in renal function, oxidative stress and apoptotic markers compared to medium and high doses.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100162"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144917690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The story so far………- current opinion in the use and applications of interactive storytelling in physiology and clinical education 迄今为止的故事.........--当前在生理学和临床教育中使用和应用互动故事的观点

IF 2.1 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100142

Bagley L. , Wilson J. , Kime A.

Physiology and clinical practice are subjects of study which demand integration of multiple sources of systems working knowledge and information on the performance of those systems to come to meaningful conclusions. This is made more complex by the interpretation and actions as a result of this conclusion having direct impact on the sum of the component systems, the human, thereby integrating significant social and psychological considerations into an already complex situation.

As higher education educators, it is a significant challenge to provide our learners with training and most importantly, practice, in these knowledge, skills and behaviours in the classroom. There has been a significant interest in recent years in providing active learning opportunities which allow learners to apply subject knowledge to multi-faceted, immersive, continuously evolving stories which reflect a graduate's professional aspirations. This review highlights practices from the literature of storytelling education which the higher education educator can utilise in promoting “meaning making” in the classroom. Here, the case for interactive storytelling in physiology and clinical education is argued, as well as presenting commonly utilised techniques and practices with which educators can embed storytelling into their pedagogy as well as highlighting future directions in this field.

生理学和临床实践是研究的主题，需要整合系统的多个来源，工作知识和信息，这些系统的性能来得出有意义的结论。由于这一结论直接影响到组成系统的总和，即人类，从而将重要的社会和心理因素整合到已经复杂的情况中，因此解释和行动使情况变得更加复杂。作为高等教育的教育者，为我们的学习者提供培训，最重要的是，在课堂上实践这些知识、技能和行为，是一项重大挑战。近年来，人们对提供主动学习机会非常感兴趣，这种机会使学习者能够将学科知识应用于反映毕业生职业抱负的多方面、沉浸式、不断发展的故事中。本文从讲故事教育的文献中总结了高等教育教育者在课堂上促进“意义创造”的实践。本文讨论了互动讲故事在生理学和临床教育中的应用，并提出了常用的技术和实践，教育工作者可以通过这些技术和实践将讲故事融入到他们的教学中，同时强调了这一领域的未来发展方向。

{"title":"The story so far………- current opinion in the use and applications of interactive storytelling in physiology and clinical education","authors":"Bagley L. , Wilson J. , Kime A.","doi":"10.1016/j.crphys.2025.100142","DOIUrl":"10.1016/j.crphys.2025.100142","url":null,"abstract":"<div><div>Physiology and clinical practice are subjects of study which demand integration of multiple sources of systems working knowledge and information on the performance of those systems to come to meaningful conclusions. This is made more complex by the interpretation and actions as a result of this conclusion having direct impact on the sum of the component systems, the human, thereby integrating significant social and psychological considerations into an already complex situation.</div><div>As higher education educators, it is a significant challenge to provide our learners with training and most importantly, practice, in these knowledge, skills and behaviours in the classroom. There has been a significant interest in recent years in providing active learning opportunities which allow learners to apply subject knowledge to multi-faceted, immersive, continuously evolving stories which reflect a graduate's professional aspirations. This review highlights practices from the literature of storytelling education which the higher education educator can utilise in promoting “meaning making” in the classroom. Here, the case for interactive storytelling in physiology and clinical education is argued, as well as presenting commonly utilised techniques and practices with which educators can embed storytelling into their pedagogy as well as highlighting future directions in this field.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100142"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143594159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microvascular endothelial cells display organ-specific responses to extracellular matrix stiffness 微血管内皮细胞对细胞外基质硬度表现出器官特异性反应

IF 2.1 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100140

Rana Haidari , Wesley J. Fowler , Stephen D. Robinson , Robert T. Johnson , Derek T. Warren

The extracellular matrix was originally thought of as simply a cellular scaffold but is now considered a key regulator of cell function and phenotype from which cells can derive biochemical and mechanical stimuli. Age-associated changes in matrix composition drive increases in matrix stiffness. Enhanced matrix stiffness promotes the progression of numerous diseases including cardiovascular disease, musculoskeletal disease, fibrosis, and cancer. Macrovascular endothelial cells undergo endothelial dysfunction in response to enhanced matrix stiffness. However, endothelial cells are highly heterogeneous, adopting structural and gene expression profiles specific to their organ of origin. Endothelial cells isolated from different vessels (i.e. arteries, veins or capillaries) respond differently to changes in substrate stiffness. It is unknown whether microvascular endothelial cells isolated from different organs also display organ-specific responses to substrate stiffness. In this study, we compare the response of microvascular endothelial cells isolated from both the mouse lung and mammary gland to a range of physiologically relevant substrate stiffnesses. We find that endothelial origin influences microvascular endothelial cell response to substrate stiffness in terms of both proliferation and migration speed. In lung-derived endothelial cells, proliferation is bimodal, where both physiologically soft and stiff substrates drive enhanced proliferation. Conversely, in mammary gland-derived endothelial cells, proliferation increases as substrate stiffness increases. Substrate stiffness also promotes enhanced endothelial migration. Enhanced stiffness drove greater increases in migration speed in mammary gland-derived than lung-derived endothelial cells. However, stiffness-induced changes in microvascular endothelial cell morphology were consistent between both cell lines, with substrate stiffness driving an increase in endothelial volume. Our research demonstrates the importance of considering endothelial origin in experimental design, especially when investigating how age-associated changes in matrix stiffness drive endothelial dysfunction and disease progression.

细胞外基质最初被认为是简单的细胞支架，但现在被认为是细胞功能和表型的关键调节剂，细胞可以从中获得生化和机械刺激。与年龄相关的基体成分变化驱动基体刚度的增加。增强的基质刚度促进了许多疾病的进展，包括心血管疾病、肌肉骨骼疾病、纤维化和癌症。大血管内皮细胞发生内皮功能障碍，以响应增强基质刚度。然而，内皮细胞是高度异质的，采用其起源器官特异性的结构和基因表达谱。从不同血管（如动脉、静脉或毛细血管）分离的内皮细胞对底物硬度的变化反应不同。目前尚不清楚从不同器官分离的微血管内皮细胞是否也表现出对底物硬度的器官特异性反应。在这项研究中，我们比较了从小鼠肺和乳腺分离的微血管内皮细胞对一系列生理相关底物刚度的反应。我们发现内皮来源影响微血管内皮细胞在增殖和迁移速度方面对底物刚度的反应。在肺源性内皮细胞中，增殖是双峰的，其中生理上柔软和坚硬的底物都驱动增殖增强。相反，在乳腺来源的内皮细胞中，随着基质硬度的增加，增殖也会增加。基质刚度也促进内皮细胞的迁移。与肺源性内皮细胞相比，乳腺源性内皮细胞的刚度增强导致了更大的迁移速度增加。然而，刚度诱导的微血管内皮细胞形态变化在两种细胞系之间是一致的，底物刚度驱动内皮细胞体积的增加。我们的研究证明了在实验设计中考虑内皮起源的重要性，特别是在研究与年龄相关的基质刚度变化如何驱动内皮功能障碍和疾病进展时。

{"title":"Microvascular endothelial cells display organ-specific responses to extracellular matrix stiffness","authors":"Rana Haidari , Wesley J. Fowler , Stephen D. Robinson , Robert T. Johnson , Derek T. Warren","doi":"10.1016/j.crphys.2025.100140","DOIUrl":"10.1016/j.crphys.2025.100140","url":null,"abstract":"<div><div>The extracellular matrix was originally thought of as simply a cellular scaffold but is now considered a key regulator of cell function and phenotype from which cells can derive biochemical and mechanical stimuli. Age-associated changes in matrix composition drive increases in matrix stiffness. Enhanced matrix stiffness promotes the progression of numerous diseases including cardiovascular disease, musculoskeletal disease, fibrosis, and cancer. Macrovascular endothelial cells undergo endothelial dysfunction in response to enhanced matrix stiffness. However, endothelial cells are highly heterogeneous, adopting structural and gene expression profiles specific to their organ of origin. Endothelial cells isolated from different vessels (i.e. arteries, veins or capillaries) respond differently to changes in substrate stiffness. It is unknown whether microvascular endothelial cells isolated from different organs also display organ-specific responses to substrate stiffness. In this study, we compare the response of microvascular endothelial cells isolated from both the mouse lung and mammary gland to a range of physiologically relevant substrate stiffnesses. We find that endothelial origin influences microvascular endothelial cell response to substrate stiffness in terms of both proliferation and migration speed. In lung-derived endothelial cells, proliferation is bimodal, where both physiologically soft and stiff substrates drive enhanced proliferation. Conversely, in mammary gland-derived endothelial cells, proliferation increases as substrate stiffness increases. Substrate stiffness also promotes enhanced endothelial migration. Enhanced stiffness drove greater increases in migration speed in mammary gland-derived than lung-derived endothelial cells. However, stiffness-induced changes in microvascular endothelial cell morphology were consistent between both cell lines, with substrate stiffness driving an increase in endothelial volume. Our research demonstrates the importance of considering endothelial origin in experimental design, especially when investigating how age-associated changes in matrix stiffness drive endothelial dysfunction and disease progression.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100140"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143134703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms involved in aminoacidurias: impacts of genetic and environmental factors 氨基酸代谢的机制：遗传和环境因素的影响

IF 1.7 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100168

Joseph Abayomi Ajayi , Evelyn Nnashiru Ananias , Muneerah Issa-Lawal , Abdulkadir Mashood Gambari , Adetoun Bunmi Aribatise , Lekan Sheriff Ojulari , Abdullateef Isiaka Alagbonsi

Background

Amino acids play vital roles in protein synthesis, energy metabolism, and cellular function. Aminoacidurias are metabolic disorders characterized by excessive urinary excretion of amino acids resulting from defects in renal tubular reabsorption or amino acid metabolism. These disorders result from a combination of genetic mutations affecting transporter proteins and environmental factors that influence disease severity. This review aims to explore the molecular mechanisms by which genetic and environmental factors disrupt amino acid homeostasis.

Methods

A scoping review was conducted following Arksey and O'Malley's framework. Relevant literature from 1980 to 2025 was identified using the PubMed and Google Scholar databases. Studies reporting genes or genetic variants, as well as environmental factors associated with aminoacidurias in humans and animals, were included.

Results

The review highlighted 9 genes associated with aminoacidurias, including SLC3A1 (rBAT), SLC7A9 (b^o,+AT), SLC6A19 (B^oAT1), SLC7A7 (y⁺LAT1), SLC7A6 (y⁺LAT2), SLC36A2 (PAT-2), SLC6A20 (SIT-1), SLC6A18 (B^oAT3), and SLC1A1 (EAAT3). Over 350 gene mutations responsible for aminoacidurias were identified. Environmental factors, including dietary intake (such as Vitamin D deficiency), gut microbiota and dysbiosis, drugs and heavy metal exposure (specifically Lead and Cadmium), were also found to cause aminoacidurias.

Conclusion

Understanding the genetic and environmental mechanisms underlying aminoacidurias is crucial for improving diagnostic strategies and developing targeted therapeutic approaches. Our findings reveal that aminoacidurias are largely influenced by genetic factors, with few environmental factors implicated in the pathophysiology of aminoacidurias. Future research should focus on gene-environment interactions and developing novel therapies targeting specific amino acid transport pathways to enhance treatment outcomes for affected individuals.

氨基酸在蛋白质合成、能量代谢和细胞功能中起着重要作用。氨基酸尿症是一种代谢性疾病，其特征是由于肾小管重吸收或氨基酸代谢缺陷导致尿中氨基酸排泄过多。这些疾病是影响转运蛋白的基因突变和影响疾病严重程度的环境因素共同作用的结果。本文旨在探讨遗传和环境因素破坏氨基酸稳态的分子机制。方法根据Arksey和O'Malley的框架进行范围审查。1980年至2025年的相关文献通过PubMed和谷歌Scholar数据库进行鉴定。研究报告了基因或遗传变异，以及与人类和动物氨基酸血症相关的环境因素。结果共筛选到9个与氨基酸血症相关的基因，包括SLC3A1 （rBAT）、SLC7A9 （bo,+AT）、SLC6A19 （BoAT1）、SLC7A7 （y+LAT1）、SLC7A6 （y+LAT2）、SLC36A2 （PAT-2）、SLC6A20 （SIT-1）、SLC6A18 （BoAT3）和SLC1A1 （EAAT3）。超过350个基因突变负责氨基酸血症鉴定。环境因素，包括饮食摄入（如维生素D缺乏）、肠道微生物群和生态失调、药物和重金属暴露（特别是铅和镉），也被发现会导致氨基酸尿症。结论了解氨基酸尿症的遗传和环境机制对改进诊断策略和开发靶向治疗方法至关重要。我们的研究结果表明，氨基酸性尿症主要受遗传因素的影响，而环境因素在氨基酸性尿症的病理生理中所起的作用很小。未来的研究应关注基因与环境的相互作用，并开发针对特定氨基酸转运途径的新疗法，以提高患者的治疗效果。

{"title":"Mechanisms involved in aminoacidurias: impacts of genetic and environmental factors","authors":"Joseph Abayomi Ajayi , Evelyn Nnashiru Ananias , Muneerah Issa-Lawal , Abdulkadir Mashood Gambari , Adetoun Bunmi Aribatise , Lekan Sheriff Ojulari , Abdullateef Isiaka Alagbonsi","doi":"10.1016/j.crphys.2025.100168","DOIUrl":"10.1016/j.crphys.2025.100168","url":null,"abstract":"<div><h3>Background</h3><div>Amino acids play vital roles in protein synthesis, energy metabolism, and cellular function. Aminoacidurias are metabolic disorders characterized by excessive urinary excretion of amino acids resulting from defects in renal tubular reabsorption or amino acid metabolism. These disorders result from a combination of genetic mutations affecting transporter proteins and environmental factors that influence disease severity. This review aims to explore the molecular mechanisms by which genetic and environmental factors disrupt amino acid homeostasis.</div></div><div><h3>Methods</h3><div>A scoping review was conducted following Arksey and O'Malley's framework. Relevant literature from 1980 to 2025 was identified using the PubMed and Google Scholar databases. Studies reporting genes or genetic variants, as well as environmental factors associated with aminoacidurias in humans and animals, were included.</div></div><div><h3>Results</h3><div>The review highlighted 9 genes associated with aminoacidurias, including SLC3A1 (rBAT), SLC7A9 (b<sup>o,+</sup>AT), SLC6A19 (B<sup>o</sup>AT1), SLC7A7 (y<sup>+</sup>LAT1), SLC7A6 (y<sup>+</sup>LAT2), SLC36A2 (PAT-2), SLC6A20 (SIT-1), SLC6A18 (B<sup>o</sup>AT3), and SLC1A1 (EAAT3). Over 350 gene mutations responsible for aminoacidurias were identified. Environmental factors, including dietary intake (such as Vitamin D deficiency), gut microbiota and dysbiosis, drugs and heavy metal exposure (specifically Lead and Cadmium), were also found to cause aminoacidurias.</div></div><div><h3>Conclusion</h3><div>Understanding the genetic and environmental mechanisms underlying aminoacidurias is crucial for improving diagnostic strategies and developing targeted therapeutic approaches. Our findings reveal that aminoacidurias are largely influenced by genetic factors, with few environmental factors implicated in the pathophysiology of aminoacidurias. Future research should focus on gene-environment interactions and developing novel therapies targeting specific amino acid transport pathways to enhance treatment outcomes for affected individuals.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100168"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145265094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Carnosine ameliorates dexamethasone-induced muscle atrophy with associated modulation of ubiquitin ligases and oxidative stress in C57BL/6J female mice 肌肽通过调节C57BL/6J雌性小鼠的泛素连接酶和氧化应激，改善地塞米松诱导的肌肉萎缩

IF 1.7 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100169

Md Mizanur Rahman , Anayt Ulla , Honomi Ogura , Haruka Tsuda , Takayuki Uchida , Tomoya Fukawa , Takeshi Nikawa

Muscle atrophy, characterized by a decline in muscle mass and function, has limited treatment options, highlighting the need for further research. In this study, we investigated the effect of carnosine, a dipeptide with well-established antioxidant properties, on dexamethasone (Dex)-induced muscle atrophy in female C57BL/6J mice. Dex (10 mg/kg body weight) reduced muscle weight, cross-sectional area (CSA), and myosin heavy chain (MyHC) protein expression, while elevating the expression of the muscle atrophy–related ubiquitin ligases Atrogin-1 and Muscle RING-finger protein-1 (MuRF1). Dex also increased oxidative stress, leading to upregulation of the oxidative stress–sensitive ubiquitin ligase Cbl-b and downregulation of IRS-1. Notably, a 21-day treatment with carnosine (300 mg/kg body weight) significantly mitigated Dex-induced reductions in muscle mass, myofiber CSA, and MyHC protein, while suppressing ubiquitin ligase expression and preserving IRS-1 levels. Carnosine likewise decreased oxidative stress and the associated Cbl-b upregulation. These findings suggest that carnosine is a promising therapeutic candidate for managing Dex-induced muscle atrophy.

肌肉萎缩以肌肉质量和功能下降为特征，其治疗选择有限，因此需要进一步研究。在这项研究中，我们研究了肌肽（一种具有良好抗氧化特性的二肽）对地塞米松（Dex）诱导的雌性C57BL/6J小鼠肌肉萎缩的影响。Dex （10 mg/kg体重）降低了肌肉质量、横截面面积（CSA）和肌球蛋白重链（MyHC）蛋白的表达，同时提高了肌萎缩相关的泛素连接酶Atrogin-1和muscle RING-finger protein-1 （MuRF1）的表达。右美托明还增加了氧化应激，导致氧化应激敏感的泛素连接酶ccl -b上调，IRS-1下调。值得注意的是，21天的肌肽治疗（300 mg/kg体重）显著减轻了dex诱导的肌肉质量、肌纤维CSA和MyHC蛋白的减少，同时抑制了泛素连接酶的表达并保持了IRS-1水平。肌肽同样降低氧化应激和相关的ccl -b上调。这些发现表明肌肽是一种很有希望的治疗药物，可以治疗dex诱导的肌肉萎缩。

{"title":"Carnosine ameliorates dexamethasone-induced muscle atrophy with associated modulation of ubiquitin ligases and oxidative stress in C57BL/6J female mice","authors":"Md Mizanur Rahman , Anayt Ulla , Honomi Ogura , Haruka Tsuda , Takayuki Uchida , Tomoya Fukawa , Takeshi Nikawa","doi":"10.1016/j.crphys.2025.100169","DOIUrl":"10.1016/j.crphys.2025.100169","url":null,"abstract":"<div><div>Muscle atrophy, characterized by a decline in muscle mass and function, has limited treatment options, highlighting the need for further research. In this study, we investigated the effect of carnosine, a dipeptide with well-established antioxidant properties, on dexamethasone (Dex)-induced muscle atrophy in female C57BL/6J mice. Dex (10 mg/kg body weight) reduced muscle weight, cross-sectional area (CSA), and myosin heavy chain (MyHC) protein expression, while elevating the expression of the muscle atrophy–related ubiquitin ligases Atrogin-1 and Muscle RING-finger protein-1 (MuRF1). Dex also increased oxidative stress, leading to upregulation of the oxidative stress–sensitive ubiquitin ligase Cbl-b and downregulation of IRS-1. Notably, a 21-day treatment with carnosine (300 mg/kg body weight) significantly mitigated Dex-induced reductions in muscle mass, myofiber CSA, and MyHC protein, while suppressing ubiquitin ligase expression and preserving IRS-1 levels. Carnosine likewise decreased oxidative stress and the associated Cbl-b upregulation. These findings suggest that carnosine is a promising therapeutic candidate for managing Dex-induced muscle atrophy.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100169"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145323790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The senescent synapse: A look at autophagy, calcium handling, and mitochondrial bioenergetics at the synapse in ageing and Parkinson's disease 衰老突触：衰老和帕金森病中突触的自噬、钙处理和线粒体生物能量学的研究

IF 1.7 Q3 PHYSIOLOGY

Current research in physiology

Pub Date : 2025-01-01 DOI: 10.1016/j.crphys.2025.100166

Shahzabe Mukhtar , Shikha Kataria , Gloria Cimaglia , Dayne Beccano-Kelly

The synapse is a vitally important physiological structure fundamental to electrochemical communication between neurones, and is required for basic and important functions we perform daily. Underpinning the normal physiological function of the synapse are crucial processes such as autophagy, calcium homeostasis, and mitochondrial bioenergetics, all of which are modified during ageing. It is necessary to understand how ageing affects these processes at the synapse, from a fundamental need to understand natural ageing, and in order to identify how these processes may become aberrant and indeed, pathological, in the context of ageing-related disorders, such as Parkinson's. This review addresses the importance of the aforementioned processes, autophagy, calcium homeostasis, and mitochondrial bioenergetics at the synapse in normal physiology, and discusses how they are altered during ageing, and in Parkinson's, an example of accelerated ageing.

突触是神经元间电化学交流的重要生理结构，是我们日常生活中所必需的基本和重要功能。支撑突触正常生理功能的是关键过程，如自噬、钙稳态和线粒体生物能量学，所有这些都在衰老过程中被改变。从理解自然衰老的基本需求出发，有必要了解衰老如何影响突触中的这些过程，以便确定这些过程如何在与衰老相关的疾病（如帕金森病）的背景下变得异常甚至是病态。这篇综述阐述了上述过程的重要性，自噬、钙稳态和线粒体生物能量在正常生理突触中的重要性，并讨论了它们在衰老过程中是如何改变的，在帕金森症中，这是一个加速衰老的例子。

引用次数: 0