I. Aggeletopoulou, C. Konstantakis, Christos Triantos
Vitamin D possesses a crucial role in preserving bone health, modulating the immune system responses, and supporting various physiological functions throughout the body. Chronic atrophic autoimmune gastritis (CAAG) constitutes an autoimmune condition marked by inflammation and damage to the stomach cells, often resulting in a decreased ability to absorb certain nutrients, including vitamin B12 and iron. Although, vitamin D is not directly affected by this condition, the sufficiency of this micronutrient seems to have important implications for overall health and management of the disease. The aim of the current review was to assess the incidence and related features of vitamin D deficiency in patients with CAAG and to elucidate the complex regulatory role of this nutrient, in an effort to improve patient outcomes. Vitamin D greatly contributes to the regulation of the immune system. In patients with CAAG, the immune system attacks the stomach lining; thus, the maintenance of a healthy and balanced immune response is important. In autoimmune conditions such as CAAG, where inflammation plays a decisive role in disease progression, vitamin D could potentially exert a role in managing and controlling the associated symptoms. Adequate vitamin D levels may help in regulating the immune response and reducing inflammation. In addition, patients with CAAG are at risk of nutrient deficiencies, including vitamin B12 and iron, which can lead to anemia and bone health issues. As vitamin D is critical for calcium absorption and bone health, assurance of sufficient levels of this micronutrient can be beneficial in preventing or mitigating bone-related complications. In conclusion, regular monitoring of vitamin D levels, among other nutrients, and appropriate supplementation, when necessary, can help improve overall health and well-being in these patients.
维生素 D 在保护骨骼健康、调节免疫系统反应和支持全身各种生理功能方面发挥着至关重要的作用。慢性萎缩性自身免疫性胃炎（CAAG）是一种以炎症和胃细胞损伤为特征的自身免疫性疾病，通常会导致吸收某些营养物质（包括维生素 B12 和铁）的能力下降。虽然维生素 D 并不直接受这种疾病的影响，但这种微量营养素的充足与否似乎对整体健康和疾病的治疗有重要影响。本综述旨在评估 CAAG 患者维生素 D 缺乏症的发病率和相关特征，并阐明这种营养素的复杂调节作用，从而改善患者的预后。维生素 D 对免疫系统的调节有很大作用。CAAG 患者的免疫系统会攻击胃黏膜；因此，维持健康、平衡的免疫反应非常重要。在 CAAG 等自身免疫性疾病中，炎症在疾病进展中起着决定性作用，维生素 D 有可能在管理和控制相关症状方面发挥作用。充足的维生素 D 水平可能有助于调节免疫反应和减轻炎症。此外，CAAG 患者有可能缺乏营养，包括维生素 B12 和铁，从而导致贫血和骨骼健康问题。由于维生素 D 对钙的吸收和骨骼健康至关重要，因此保证这种微量营养素的充足水平有利于预防或减轻与骨骼相关的并发症。总之，定期监测维生素 D 和其他营养素的水平，并在必要时适当补充，有助于改善这些患者的整体健康和福祉。
{"title":"Chronic Atrophic Autoimmune Gastritis: The Evolving Role of Vitamin D","authors":"I. Aggeletopoulou, C. Konstantakis, Christos Triantos","doi":"10.31083/j.fbl2907252","DOIUrl":"https://doi.org/10.31083/j.fbl2907252","url":null,"abstract":"Vitamin D possesses a crucial role in preserving bone health, modulating the immune system responses, and supporting various physiological functions throughout the body. Chronic atrophic autoimmune gastritis (CAAG) constitutes an autoimmune condition marked by inflammation and damage to the stomach cells, often resulting in a decreased ability to absorb certain nutrients, including vitamin B12 and iron. Although, vitamin D is not directly affected by this condition, the sufficiency of this micronutrient seems to have important implications for overall health and management of the disease. The aim of the current review was to assess the incidence and related features of vitamin D deficiency in patients with CAAG and to elucidate the complex regulatory role of this nutrient, in an effort to improve patient outcomes. Vitamin D greatly contributes to the regulation of the immune system. In patients with CAAG, the immune system attacks the stomach lining; thus, the maintenance of a healthy and balanced immune response is important. In autoimmune conditions such as CAAG, where inflammation plays a decisive role in disease progression, vitamin D could potentially exert a role in managing and controlling the associated symptoms. Adequate vitamin D levels may help in regulating the immune response and reducing inflammation. In addition, patients with CAAG are at risk of nutrient deficiencies, including vitamin B12 and iron, which can lead to anemia and bone health issues. As vitamin D is critical for calcium absorption and bone health, assurance of sufficient levels of this micronutrient can be beneficial in preventing or mitigating bone-related complications. In conclusion, regular monitoring of vitamin D levels, among other nutrients, and appropriate supplementation, when necessary, can help improve overall health and well-being in these patients.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141830540","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}
Sonia Carta, Maddalena Ghelardoni, Francesca Vitale, Silvia Ravera, Vanessa Cossu, N. Bertola, Serena Losacco, Jonathan Martinelli, Edoardo Dighero, M. Riondato, A. Orengo, Matteo Bauckneht, Sabrina Chiesa, G. Sambuceti, Cecilia Marini
Background : Selective deprivation of glutamine has been shown to accelerate the generation of reactive oxygen species (ROS) and to impair the activity of a specific pentose phosphate pathway (PPP) located within the endoplasmic reticulum (ER). The consequent oxidative damage suggests that glucose flux through this reticular pathway might contribute to the redox stress of breast cancer cells. We thus evaluated whether this response is reproduced when the glutamine shortage is coupled with the glucose deprivation. Methods : Cancer growth, metabolic plasticity and redox status were evaluated under saturating conditions and after 48 h starvation (glucose 2.5 mM, glutamine 0.5 mM). The Seahorse technology was used to estimate adenosine triphosphate (ATP)-linked and ATP-independent oxygen consumption rate (OCR) as well as proton efflux rate (PER). 18 F-fluoro-deoxy-glucose (FDG) uptake was evaluated through the LigandTracer device. Proliferation rate was estimated by the carboxyfluorescein-diacetate-succinimidyl ester (CFSE) staining, while cell viability by the propidium iodide exclusion assay. Results : Starvation reduced the proliferation rate of MCF-7 cells without affecting their viability. It also decreased lactate release and PER. Overall OCR was left unchanged although ATP-synthase dependent fraction was increased under nutrient shortage. Glutaminolysis inhibition selectively impaired the ATP-independent and the oligomycin-sensitive OCR in control and starved cultures, respectively. The combined nutrient shortage decreased the cytosolic and mitochondrial markers of redox stress. It also left unchanged the expression of the reticular unfolded protein marker GRP78. By contrast, starvation decreased the expression of hexose-6P-dehydrogenase (H6PD) thus decreasing the glucose flux through the ER-PPP as documented by the profound impairment in the uptake rate of FDG. Conclusions : When combined with glucose deprivation, glutamine shortage does not elicit the expected enhancement of ROS generation in the studied breast cancer cell line. Combined with the decreased activity of ER-PPP, this observation suggests that glutamine interferes with the reticular glucose metabolism to regulate the cell redox balance.
背景：研究表明，选择性地剥夺谷氨酰胺会加速活性氧（ROS）的生成，并损害位于内质网（ER）内的特定磷酸戊糖通路（PPP）的活性。由此产生的氧化损伤表明，通过这一网状途径的葡萄糖通量可能会导致乳腺癌细胞的氧化还原压力。因此，我们评估了在谷氨酰胺短缺和葡萄糖被剥夺的情况下，这种反应是否会重现。方法：在饱和条件下和饥饿 48 小时后（葡萄糖 2.5 mM，谷氨酰胺 0.5 mM），对癌症生长、代谢可塑性和氧化还原状态进行评估。海马技术用于估算与三磷酸腺苷（ATP）相关和与 ATP 无关的耗氧率（OCR）以及质子外流率（PER）。18 F-氟脱氧葡萄糖（FDG）摄取量通过 LigandTracer 设备进行评估。细胞增殖率通过羧基荧光素-二乙酸琥珀酰亚胺酯（CFSE）染色法进行评估，细胞存活率则通过碘化丙啶排除法进行评估。结果：饥饿降低了 MCF-7 细胞的增殖率，但不影响其存活率。饥饿还减少了乳酸释放和 PER。虽然 ATP 合成酶依赖部分在营养缺乏时有所增加，但总体 OCR 保持不变。谷氨酰胺溶解抑制分别选择性地损害了对照组和饥饿培养物中不依赖 ATP 的 OCR 和对寡霉素敏感的 OCR。综合营养短缺降低了氧化还原压力的细胞膜和线粒体标记。它还使网状结构未折叠蛋白标记物 GRP78 的表达保持不变。与此相反，饥饿降低了己糖-6P-脱氢酶（H6PD）的表达，从而降低了通过ER-PPP的葡萄糖通量，FDG吸收率的显著下降就证明了这一点。结论 ：在研究的乳腺癌细胞系中，谷氨酰胺短缺与葡萄糖剥夺相结合时，并不会引起预期的 ROS 生成增加。结合ER-PPP活性的降低，这一观察结果表明谷氨酰胺干扰了网状结构的葡萄糖代谢，从而调节了细胞的氧化还原平衡。
{"title":"The Glucose-Glutamine Metabolic Interplay in MCF-7 Cells, a Hormone-Sensitive Breast Cancer Model","authors":"Sonia Carta, Maddalena Ghelardoni, Francesca Vitale, Silvia Ravera, Vanessa Cossu, N. Bertola, Serena Losacco, Jonathan Martinelli, Edoardo Dighero, M. Riondato, A. Orengo, Matteo Bauckneht, Sabrina Chiesa, G. Sambuceti, Cecilia Marini","doi":"10.31083/j.fbl2907251","DOIUrl":"https://doi.org/10.31083/j.fbl2907251","url":null,"abstract":"Background : Selective deprivation of glutamine has been shown to accelerate the generation of reactive oxygen species (ROS) and to impair the activity of a specific pentose phosphate pathway (PPP) located within the endoplasmic reticulum (ER). The consequent oxidative damage suggests that glucose flux through this reticular pathway might contribute to the redox stress of breast cancer cells. We thus evaluated whether this response is reproduced when the glutamine shortage is coupled with the glucose deprivation. Methods : Cancer growth, metabolic plasticity and redox status were evaluated under saturating conditions and after 48 h starvation (glucose 2.5 mM, glutamine 0.5 mM). The Seahorse technology was used to estimate adenosine triphosphate (ATP)-linked and ATP-independent oxygen consumption rate (OCR) as well as proton efflux rate (PER). 18 F-fluoro-deoxy-glucose (FDG) uptake was evaluated through the LigandTracer device. Proliferation rate was estimated by the carboxyfluorescein-diacetate-succinimidyl ester (CFSE) staining, while cell viability by the propidium iodide exclusion assay. Results : Starvation reduced the proliferation rate of MCF-7 cells without affecting their viability. It also decreased lactate release and PER. Overall OCR was left unchanged although ATP-synthase dependent fraction was increased under nutrient shortage. Glutaminolysis inhibition selectively impaired the ATP-independent and the oligomycin-sensitive OCR in control and starved cultures, respectively. The combined nutrient shortage decreased the cytosolic and mitochondrial markers of redox stress. It also left unchanged the expression of the reticular unfolded protein marker GRP78. By contrast, starvation decreased the expression of hexose-6P-dehydrogenase (H6PD) thus decreasing the glucose flux through the ER-PPP as documented by the profound impairment in the uptake rate of FDG. Conclusions : When combined with glucose deprivation, glutamine shortage does not elicit the expected enhancement of ROS generation in the studied breast cancer cell line. Combined with the decreased activity of ER-PPP, this observation suggests that glutamine interferes with the reticular glucose metabolism to regulate the cell redox balance.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 20","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141831562","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}
Jing Luo, Hongmei Yu, Zhen Yuan, Wenqing Tang, Chen Wang
{"title":"REST Promotes Autophagy in Gastric Cancer by Transcriptionally Activating FABP6 to Inhibit the Akt/mTOR Signaling Pathway","authors":"Jing Luo, Hongmei Yu, Zhen Yuan, Wenqing Tang, Chen Wang","doi":"10.31083/j.fbl2906212","DOIUrl":"https://doi.org/10.31083/j.fbl2906212","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"84 13","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141352785","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}
Xiao-Yan Pu, Yonghong Mei, Qiang Zheng, Chih-Yuan Ko
Background : This study investigated the impact of salvianolic acids, derived from Danshen, on melanoma cell growth. Specifically, we assessed the ability of salvianolic acid A (Sal A) to modulate melanoma cell proliferation. Methods : We used human melanoma A2058 and A375 cell lines to investigate the effects of Sal A on cell proliferation and death by measuring bromodeoxyuridine incorporation and lactate dehydrogenase release. We assessed cell viability and cycle progression using water soluble tetrazolium salt-1 (WST-1) mitochondrial staining and propidium iodide. Additionally, we used a phospho-kinase array to investigate intracellular kinase phosphorylation, specifically measuring the influence of Sal A on checkpoint kinase-2 (Chk-2) via western blot analysis. Results : Sal A inhibited the growth of A2058 and A375 cells dose-responsively and induced cell cycle arrest at the G2/M phase. Notably, Sal A selectively induces Chk-2 phosphorylation without affecting Chk-1, thereby degrading Chk-2-regulated genes Cdc25A and Cdc2 . However, Sal A does not affect the Chk1-Cdc25C pathway. Conclusions : Salvianolic acids, especially Sal A, effectively hinder melanoma cell growth by inducing Chk-2 phosphorylation and disrupting G2/M checkpoint regulation.
背景：本研究调查了从丹参中提取的丹酚酸对黑色素瘤细胞生长的影响。具体来说，我们评估了丹参酚酸 A（Sal A）调节黑色素瘤细胞增殖的能力。方法：我们利用人体黑色素瘤 A2058 和 A375 细胞系，通过测量溴脱氧尿苷掺入量和乳酸脱氢酶释放量，研究 Sal A 对细胞增殖和死亡的影响。我们使用水溶性四氮唑盐-1（WST-1）线粒体染色和碘化丙啶评估细胞活力和周期进展。此外，我们还使用磷酸激酶阵列来研究细胞内激酶的磷酸化，特别是通过 Western 印迹分析来测量 Sal A 对检查点激酶-2（Chk-2）的影响。结果：Sal A能剂量反应性地抑制A2058和A375细胞的生长，并诱导细胞周期停滞在G2/M期。值得注意的是，Sal A可选择性地诱导Chk-2磷酸化，而不影响Chk-1，从而降解Chk-2调控基因Cdc25A和Cdc2。然而，Sal A 并不影响 Chk1-Cdc25C 通路。结论 ：丹酚酸，尤其是丹酚酸 A，通过诱导 Chk-2 磷酸化和破坏 G2/M 检查点调控，有效阻碍了黑色素瘤细胞的生长。
{"title":"Inhibition of Melanoma Cell Growth by Salvianolic Acid A through CHK2-CDC25A Pathway Modulation","authors":"Xiao-Yan Pu, Yonghong Mei, Qiang Zheng, Chih-Yuan Ko","doi":"10.31083/j.fbl2906213","DOIUrl":"https://doi.org/10.31083/j.fbl2906213","url":null,"abstract":"Background : This study investigated the impact of salvianolic acids, derived from Danshen, on melanoma cell growth. Specifically, we assessed the ability of salvianolic acid A (Sal A) to modulate melanoma cell proliferation. Methods : We used human melanoma A2058 and A375 cell lines to investigate the effects of Sal A on cell proliferation and death by measuring bromodeoxyuridine incorporation and lactate dehydrogenase release. We assessed cell viability and cycle progression using water soluble tetrazolium salt-1 (WST-1) mitochondrial staining and propidium iodide. Additionally, we used a phospho-kinase array to investigate intracellular kinase phosphorylation, specifically measuring the influence of Sal A on checkpoint kinase-2 (Chk-2) via western blot analysis. Results : Sal A inhibited the growth of A2058 and A375 cells dose-responsively and induced cell cycle arrest at the G2/M phase. Notably, Sal A selectively induces Chk-2 phosphorylation without affecting Chk-1, thereby degrading Chk-2-regulated genes Cdc25A and Cdc2 . However, Sal A does not affect the Chk1-Cdc25C pathway. Conclusions : Salvianolic acids, especially Sal A, effectively hinder melanoma cell growth by inducing Chk-2 phosphorylation and disrupting G2/M checkpoint regulation.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"31 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141353477","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}
L. Longhitano, D. Tibullo, T. Zuppelli, Simone Ronsisvalle, E. La Spina, Anna Nicolosi, Maria Antoci, F. Sipala, Fabio Galvano, W. Currenti, Annalisa Santisi, A. M. Alanazi, Guido Zanghì, Emanuela Tropea, Giovanni Li Volti, I. Barbagallo
Background : Nonalcoholic fatty liver disease (NAFLD) is a prevalent condition characterized by hepatic fat accumulation, often progressing to severe liver injury, for which approved treatments are currently lacking. This study explores the potential therapeutic impact of alpha-lipoic acid (ALA), a natural compound crucial in lipid metabolism, on NAFLD using an in vitro model. Methods : HepG2 cells were treated with a palmitic acid:oleic acid (PA:OA) mixture, representing a cellular model of steatosis. Subsequent treatment with ALA at concentrations of 1 µM and 5 µM aimed to evaluate its effects on lipid content and metabolism. Real-time polymerase chain reaction (PCR), BODIPY staining, cytofluorimetric analysis, and lipidomics were used to assess gene expression, lipid droplet accumulation, and fatty acid profiles. Results : Our results showed that ALA significantly reduced lipid droplets in PA:OA-treated HepG2 cells, with a concentration-dependent effect. Analysis of fatty acid profiles demonstrated a decrease in palmitic acid levels with ALA treatment, while oleic acid reduction was observed only at the higher concentration. Moreover, ALA modulated the expression of genes involved in cholesterol biosynthesis and low-density lipoprotein (LDL) metabolism, indicating a potential role in lipid homeostasis. Further insights into molecular mechanisms revealed that ALA modulated peroxisome proliferator activated receptors (PPARs), specifically PPAR-alpha and PPAR-gamma, involved in fatty acid metabolism and insulin sensitivity. Finally, ALA counteracted the overexpression of thermo-genic genes induced by exogenous fatty acids, suggesting a regulatory role in energy dissipation pathways. Conclusion : In conclusion, this study highlights ALA as a therapeutic agent in mitigating lipid accumulation and dysregulation in NAFLD.
{"title":"(+)Alpha-Lipoic Acid Regulates Lipid Metabolism Gene Expression and Lipidic Profile in a Cellular Model of Fatty Acid Overload","authors":"L. Longhitano, D. Tibullo, T. Zuppelli, Simone Ronsisvalle, E. La Spina, Anna Nicolosi, Maria Antoci, F. Sipala, Fabio Galvano, W. Currenti, Annalisa Santisi, A. M. Alanazi, Guido Zanghì, Emanuela Tropea, Giovanni Li Volti, I. Barbagallo","doi":"10.31083/j.fbl2906209","DOIUrl":"https://doi.org/10.31083/j.fbl2906209","url":null,"abstract":"Background : Nonalcoholic fatty liver disease (NAFLD) is a prevalent condition characterized by hepatic fat accumulation, often progressing to severe liver injury, for which approved treatments are currently lacking. This study explores the potential therapeutic impact of alpha-lipoic acid (ALA), a natural compound crucial in lipid metabolism, on NAFLD using an in vitro model. Methods : HepG2 cells were treated with a palmitic acid:oleic acid (PA:OA) mixture, representing a cellular model of steatosis. Subsequent treatment with ALA at concentrations of 1 µM and 5 µM aimed to evaluate its effects on lipid content and metabolism. Real-time polymerase chain reaction (PCR), BODIPY staining, cytofluorimetric analysis, and lipidomics were used to assess gene expression, lipid droplet accumulation, and fatty acid profiles. Results : Our results showed that ALA significantly reduced lipid droplets in PA:OA-treated HepG2 cells, with a concentration-dependent effect. Analysis of fatty acid profiles demonstrated a decrease in palmitic acid levels with ALA treatment, while oleic acid reduction was observed only at the higher concentration. Moreover, ALA modulated the expression of genes involved in cholesterol biosynthesis and low-density lipoprotein (LDL) metabolism, indicating a potential role in lipid homeostasis. Further insights into molecular mechanisms revealed that ALA modulated peroxisome proliferator activated receptors (PPARs), specifically PPAR-alpha and PPAR-gamma, involved in fatty acid metabolism and insulin sensitivity. Finally, ALA counteracted the overexpression of thermo-genic genes induced by exogenous fatty acids, suggesting a regulatory role in energy dissipation pathways. Conclusion : In conclusion, this study highlights ALA as a therapeutic agent in mitigating lipid accumulation and dysregulation in NAFLD.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"22 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141356769","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}
Traumatic spinal cord injury (SCI) is a serious disease of the central nervous system. Aside from the limited intrinsic regenerative capacity of neurons, complex microenvironmental disturbances can also lead to further cellular damage and growth inhibition. Programmed cell death regulated by pyroptosis has an important role in the pathogenesis of SCI. While there has been a wealth of new knowledge regarding cellular pyroptosis, a detailed understanding of its role in SCI and possible therapeutic strategies is still lacking. This review summarizes current advances in the regulatory role of pyroptosis-regulated cell death and inflammasome components in the inhibitory microenvironment following SCI, as well as recent therapeutic advances.
{"title":"Pyroptosis in Spinal Cord Injury: Implications for Pathogenesis and Therapeutic Approaches","authors":"Guangjin Gu, Huaqi Yu, Huishuang Zou, Wenjuan Kou, Pingping Zhang, Guangjie Gu, Jie Lu, Weihan Shi, Pengcheng Chu, Yaning Zhang, Guangwei Sun, Jun Shang","doi":"10.31083/j.fbl2906210","DOIUrl":"https://doi.org/10.31083/j.fbl2906210","url":null,"abstract":"Traumatic spinal cord injury (SCI) is a serious disease of the central nervous system. Aside from the limited intrinsic regenerative capacity of neurons, complex microenvironmental disturbances can also lead to further cellular damage and growth inhibition. Programmed cell death regulated by pyroptosis has an important role in the pathogenesis of SCI. While there has been a wealth of new knowledge regarding cellular pyroptosis, a detailed understanding of its role in SCI and possible therapeutic strategies is still lacking. This review summarizes current advances in the regulatory role of pyroptosis-regulated cell death and inflammasome components in the inhibitory microenvironment following SCI, as well as recent therapeutic advances.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"122 47","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141360619","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}
{"title":"A Preliminary Investigation into the Effect of Low-Energy Lasers on Dental Pulp Stem Cell Proliferation and the Associated Mechanism","authors":"Wenting Pan, Shiwen Yan, Tiantian Li, He Jiang, Mengwen Wang, Peng Xue","doi":"10.31083/j.fbl2906211","DOIUrl":"https://doi.org/10.31083/j.fbl2906211","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141357064","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}
{"title":"A Predictive Model Based on the FBXO Family Reveals the Significance of Cyclin F in Hepatocellular Carcinoma","authors":"D. Gao, Suxin Li, Huahu Guo, Xianfu Liu, Zhaochen Liu, Luhao Li, Liang Bao, Xiaowei Dang","doi":"10.31083/j.fbl2905202","DOIUrl":"https://doi.org/10.31083/j.fbl2905202","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"8 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141102695","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}
Tao Liu, Manqi Yang, Bo Cui, Hao Ju, Jinchun Wu, Zongli Ren, Sheng Cao, Min Yan, Fan Zhang, Zheyu Liu, Shuijing He, Jiajun Zhang, R. Hiram, Feng Xiong, Mian Cheng, Gang Wu
{"title":"Alterations of Myocardial Mitochondrial Morphology and Function in a Canine Model of Premature Ventricular Contractions-Induced Cardiomyopathy","authors":"Tao Liu, Manqi Yang, Bo Cui, Hao Ju, Jinchun Wu, Zongli Ren, Sheng Cao, Min Yan, Fan Zhang, Zheyu Liu, Shuijing He, Jiajun Zhang, R. Hiram, Feng Xiong, Mian Cheng, Gang Wu","doi":"10.31083/j.fbl2905200","DOIUrl":"https://doi.org/10.31083/j.fbl2905200","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"97 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141111563","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}
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