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Effects of renal denervation on the course of cardiorenal syndrome: insight from studies with fawn-hooded hypertensive rats. 肾去神经支配对心肾综合征病程的影响:来自小鹿兜帽高血压大鼠的研究。
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935469
J Doul, O Gawrys, P Škaroupková, Z Vaňourková, B Szeiffová Bačová, M Sýkora, H Maxová, L Hošková, M Šnorek, J Sadowski, M Táborský, L Červenka

Combination of chronic kidney disease (CKD) and heart failure (HF) results in extremely high morbidity and mortality. The current guideline-directed medical therapy is rarely effective and new therapeutic approaches are urgently needed. The study was designed to examine if renal denervation (RDN) will exhibit long-standing beneficial effects on the HF- and CKD-related morbidity and mortality. Fawn-hooded hypertensive rats (FHH) served as a genetic model of CKD and fawn-hooded low-pressure rats (FHL) without CKD served as controls. HF was induced by creation of aorto-caval fistula (ACF). RDN was performed 28 days after creation of ACF and the follow-up period was 70 days. ACF FHH subjected to sham-RDN had survival rate of 34 % i.e. significantly lower than 79 % observed in sham-denervated ACF FHL. RDN did not improve the condition and the final survival rate, both in ACF FHL and in ACF FHH. In FHH basal albuminuria was markedly higher than in FHL, and further increased throughout the study. RDN did not lower albuminuria and did not reduce renal glomerular damage in FHH. In these rats creation of ACF resulted in marked bilateral cardiac hypertrophy and alterations of cardiac connexin-43, however, RDN did not modify any of the cardiac parameters. Our present results further support the notion that kidney damage aggravates the HF-related morbidity and mortality. Moreover, it is clear that in the ACF FHH model of combined CKD and HF, RDN does not exhibit any important renoprotective or cardioprotective effects and does not reduce mortality. Key words Chronic kidney disease, Heart failure, Renal denervation, Fawn-hooded hypertensive rats.

慢性肾脏疾病(CKD)和心力衰竭(HF)合并导致极高的发病率和死亡率。目前的指导药物治疗很少有效,迫切需要新的治疗方法。该研究旨在检查肾去神经支配(RDN)是否会对HF和ckd相关的发病率和死亡率产生长期有益的影响。以小鹿兜高血压大鼠(FHH)为CKD遗传模型,以无CKD的小鹿兜低压大鼠(FHL)为对照组。主动脉-腔静脉瘘(ACF)诱发HF。于ACF形成后28 d进行RDN,随访70 d。假性rdn的ACF FHL存活率为34%,显著低于假性去神经ACF FHL的79%。无论是ACF FHL还是ACF FHH, RDN都没有改善病情和最终生存率。FHH组的基础蛋白尿明显高于FHL组,并且在整个研究过程中进一步增加。RDN不能降低蛋白尿,也不能减轻FHH的肾小球损害。在这些大鼠中,ACF的产生导致了明显的双侧心脏肥大和心脏连接蛋白43的改变,然而,RDN没有改变任何心脏参数。我们目前的结果进一步支持肾脏损害加重hf相关发病率和死亡率的观点。此外,很明显,在CKD和HF合并的ACF FHH模型中,RDN没有表现出任何重要的肾保护或心脏保护作用,也没有降低死亡率。【关键词】慢性肾病;心力衰竭;肾去神经支配;
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引用次数: 0
In silico validation of non-invasive arterial compliance estimation and potential determinants of its variability. 非侵入性动脉顺应性评估及其变异性的潜在决定因素的计算机验证。
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935466
M Javorka, D Švec, V Bikia, B Czippelová, N Stergiopulos, J Čerňanová Krohová

Arterial compliance (AC) is an important cardiovascular parameter characterizing mechanical properties of arteries. AC is significantly influenced by arterial wall structure and vasomotion, and it markedly influences cardiac load. A new method, based on a two-element Windkessel model, has been recently proposed for estimating AC as the ratio of the time constant T of the diastolic blood pressure decay and peripheral vascular resistance derived from clinically available stroke volume measurements and selected peripheral blood pressure parameters which are less prone to peripheral distortions. The aim of this study was to validate AC estimation using a virtual population generated by in silico model of the systemic arterial tree. In the second part of study, we analysed causal coupling between AC oscillations and variability of its potential determinants - systolic blood pressure and heart rate in healthy young human subjects. The pool of virtual subjects (n=3818) represented an extensive AC distribution. AC was estimated from the peripheral blood pressure curve and by the standard method from the aortic blood pressure curve. The proposed method slightly overestimated AC set in the model but both ACs were strongly correlated (r=0.94, p<0.001). In real data, we observed that AC dynamics was coupled with basic cardiovascular parameters variability independently of the autonomic nervous system state. In silico analysis suggests that AC can be reliably estimated by noninvasive method. The analysis of short-term AC variability together with its determinants could improve our understanding of factors involved in AC dynamics potentially improving assessment of AC changes associated with atherosclerosis process. Key words Arterial compliance, Cardiovascular model, Arterial blood pressure, Causal analysis, Volume-clamp photoplethysmography.

动脉顺应性(AC)是表征动脉力学特性的重要心血管参数。AC受动脉壁结构和血管舒缩的显著影响,并显著影响心脏负荷。最近提出了一种基于二元Windkessel模型的新方法,用于估计AC为舒张压衰减的时间常数T与外周血管阻力的比值,该比值来自临床可用的脑卒中容积测量和选择的不易引起外周扭曲的外周血压参数。本研究的目的是利用系统动脉树的计算机模型生成的虚拟种群来验证交流估计。在研究的第二部分,我们分析了健康年轻人交流振荡与其潜在决定因素——收缩压和心率变异性之间的因果耦合。虚拟受试者池(n=3818)代表广泛的AC分布。通过外周血压曲线和主动脉压曲线的标准方法估计AC。提出的方法略高估了模型中的AC集,但两个AC都是强相关的(r=0.94, p
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引用次数: 0
Risk impact of SARS-CoV-2 coronavirus and spike protein on cardiac tissue: a comprehensive review. SARS-CoV-2冠状病毒和刺突蛋白对心脏组织的风险影响:综合综述
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935476
O Šerý, R Dziedzinska

The global COVID-19 pandemic, caused by SARS-CoV-2, has led to significant morbidity and mortality, with a profound impact on cardiovascular health. This review investigates the mechanisms of SARS-CoV-2's interaction with cardiac tissue, particularly emphasizing the role of the Spike protein and ACE2 receptor in facilitating viral entry and subsequent cardiac complications. We dissect the structural features of the virus, its interactions with host cell receptors, and the resulting pathophysiological changes in the heart. Highlighting SARS-CoV-2's broad organ tropism, especially its effects on cardiomyocytes via ACE2 and TMPRSS2, the review addresses how these interactions exacerbate cardiovascular issues in patients with pre-existing conditions such as diabetes and hypertension. Additionally, we assess both direct and indirect mechanisms of virus-induced cardiac damage, including myocarditis, arrhythmias, and long-term complications such as 'long COVID'. This review underscores the complexity of SARS-CoV-2's impact on the heart, emphasizing the need for ongoing research to fully understand its long-term effects on cardiovascular health. Key words: COVID-19, Heart, ACE2, Spike protein, Cardiomyocytes, Myocarditis, Long COVID.

由SARS-CoV-2引起的全球COVID-19大流行导致了大量发病率和死亡率,对心血管健康产生了深远影响。本文综述了SARS-CoV-2与心脏组织相互作用的机制,特别强调了Spike蛋白和ACE2受体在促进病毒进入和随后的心脏并发症中的作用。我们剖析了病毒的结构特征,它与宿主细胞受体的相互作用,以及由此引起的心脏病理生理变化。该综述强调了SARS-CoV-2的广泛器官亲和性,特别是其通过ACE2和TMPRSS2对心肌细胞的影响,探讨了这些相互作用如何加剧糖尿病和高血压等既往疾病患者的心血管问题。此外,我们评估了病毒诱导的心脏损伤的直接和间接机制,包括心肌炎、心律失常和长期并发症,如“长COVID”。这一综述强调了SARS-CoV-2对心脏影响的复杂性,强调需要进行持续研究,以充分了解其对心血管健康的长期影响。关键词:COVID-19,心脏,ACE2,刺突蛋白,心肌细胞,心肌炎,长COVID
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引用次数: 0
50 years of the Czech and Slovak Society of Experimental Cardiology - historical background and scientific benefit. 捷克和斯洛伐克实验心脏病学会50年-历史背景和科学利益。
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935538
B Ostadal, M Novakova, J Slezak

The history of the Czech and Slovak experimental cardiology describes a completely unusual curve. The personality of J.E. Purkynje caused this field to reach unprecedented peak at the very beginning of its modern history. The development of experimental cardiology after the death of the great scholar was certainly not linear. Just when it seemed to be raising its head, the German occupation came. Its second hopeful awakening was delayed for a long time by forty years of isolation. The significant limitation of foreign contacts gradually led to the loss of hopefully developing contacts, to professional isolation and lagging behind the stormy development of world science. At the moment of greatest depression, in 1971, in Prague there was created a professional forum that was supposed to enable its intellectual survival and reduce the negative consequences of the "splendid isolation". The Society of Experimental Cardiology (SEC) was founded at the Czechoslovak Physiological Society of the Czechoslovak Medical Society J.E. Purkynje, with the main task of introducing theoretical and clinical cardiologists to the advances in world cardiology. The first meeting was held in 1973 and in 2023 we celebrated already the 50th anniversary of SEC. Moreover, nowadays we see the increasing interest of the young researchers, both experimental and clinical cardiologists, who consider SEC a very attractive platform for their education and professional growth. Key words: Experimental cardiology, Czech and Slovak Society, History, Relationship to clinical cardiology.

捷克和斯洛伐克实验心脏病学的历史描述了一条完全不同寻常的曲线。J.E. Purkynje的个性使这一领域在其现代史之初就达到了前所未有的高峰。这位伟大的学者死后,实验心脏病学的发展当然不是线性的。正当它似乎要抬头的时候,德国的占领来了。它第二次充满希望的觉醒被40年的孤立拖延了很长时间。对外交往的显著限制逐渐导致了有希望发展的交往的丧失,导致了专业上的孤立和落后于世界科学的迅猛发展。在1971年最严重的萧条时期,在布拉格创建了一个专业论坛,旨在使其思想得以生存,并减少“辉煌的孤立”的负面后果。实验心脏病学会(SEC)是在捷克斯洛伐克医学学会J.E. Purkynje的捷克斯洛伐克生理学会成立的,其主要任务是向理论和临床心脏病专家介绍世界心脏病学的进展。第一次会议于1973年举行,2023年我们已经庆祝了SEC成立50周年。此外,现在我们看到年轻研究人员的兴趣越来越大,无论是实验还是临床心脏病专家,他们都认为SEC是一个非常有吸引力的教育和专业成长平台。关键词:实验心脏病学,捷克斯洛伐克社会,历史,与临床心脏病学的关系
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引用次数: 0
Adipokine Levels of RBP4, Resistin and Nesfatin-1 in Women Diagnosed With Gestational Diabetes.
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31
V Kučerová, D Karásek, O Krystyník, L Štefaničková, V Němeček, D Friedecký

Gestational diabetes mellitus (GDM) is a common complication of pregnancy in which women without previously diagnosed diabetes develop chronic hyperglycemia during pregnancy. It is associated with a number of maternal and fetal/neonatal complications. The role of the adipokines retinol binding protein-4, resistin and nesfatin-1 in the development of GDM is relatively poorly understood, but their role in glucose metabolism is suspected and their use as early markers to predict the development of GDM is being sought. The aim of study was to determine the correlation between the levels of selected adipokines (retinol binding protein-4, resistin, nesfatin-1) in women with gestational diabetes mellitus (GDM) and healthy pregnant women and to compare their levels with other clinical and biochemical parameters. Patients with GDM had significantly higher BMI (28.4±4.5 vs. 24.6±4 kg/m2), total cholesterol (6±1.3 vs. 5.3±1.4 mmol/l) and triacylglycerols (1.9±0.8 vs. 1.4±0.7 mmol/l) than women in the control group. RBP4 confirms the significant difference between the groups, it is higher in the control group of healthy pregnant women. The adipokines resistin and nesfatin-1 show no differences between the control and GDM groups, but their ratios with BMI, cholesterol and triacylglycerols, resistin shows elevated levels in the control group. In women with GDM, RBP4 was significantly positively correlated with C-peptide and negatively correlated with total, LDL, and non-HDL cholesterol. Resistin was also negatively correlated with total, LDL, HDL, and non-HDL cholesterol. Nesfatin-1 was only moderately positively correlated with glycated hemoglobin (HbA1C) and fasting glycemia. There is ambiguity in the results of previous studies on the levels of the investigated adipokines in pregnant women with GDM and the interpretation depends on many factors. Keywords: Gestational diabetes, Adipokines, Retinol-binding protein 4, Resistin, Nesfatin-1.

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引用次数: 0
Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31
M Ferko, P Alanova, D Janko, B Opletalova, N Andelova

An excessive increase in reactive oxygen species (ROS) levels is one of the main causes of mitochondrial dysfunction. However, when ROS levels are maintained in balance with antioxidant mechanisms, ROS fulfill the role of signaling molecules and modulate various physiological processes. Recent advances in mitochondrial bioenergetics research have revealed a significant interplay between mitochondrial peroxiredoxins (PRDXs) and monoamine oxidase-A (MAO-A) in regulating ROS levels. Both proteins are associated with hydrogen peroxide (H2O2), MAO-A as a producer and PRDXs as the primary antioxidant scavengers of H2O2. This review focuses on the currently available knowledge on the function of these proteins and their interaction, highlighting their importance in regulating oxidative damage, apoptosis, and metabolic adaptation in the heart. PRDXs not only scavenge excess H2O2, but also act as regulatory proteins, play an active role in redox signaling, and maintain mitochondrial membrane integrity. Overexpression of MAO-A is associated with increased oxidative damage, leading to mitochondrial dysfunction and subsequent progression of cardiovascular diseases (CVD), including ischemia/reperfusion injury and heart failure. Considering the central role of oxidative damage in the pathogenesis of many CVD, targeting PRDXs activation and MAO-A inhibition may offer new therapeutic strategies aimed at improving cardiac function under conditions of pathological load related to oxidative damage. Keywords: Mitochondria, Peroxiredoxin, Monoamine oxidase-A, Reactive oxygen species, Cardioprotective signaling.

{"title":"Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.","authors":"M Ferko, P Alanova, D Janko, B Opletalova, N Andelova","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>An excessive increase in reactive oxygen species (ROS) levels is one of the main causes of mitochondrial dysfunction. However, when ROS levels are maintained in balance with antioxidant mechanisms, ROS fulfill the role of signaling molecules and modulate various physiological processes. Recent advances in mitochondrial bioenergetics research have revealed a significant interplay between mitochondrial peroxiredoxins (PRDXs) and monoamine oxidase-A (MAO-A) in regulating ROS levels. Both proteins are associated with hydrogen peroxide (H2O2), MAO-A as a producer and PRDXs as the primary antioxidant scavengers of H2O2. This review focuses on the currently available knowledge on the function of these proteins and their interaction, highlighting their importance in regulating oxidative damage, apoptosis, and metabolic adaptation in the heart. PRDXs not only scavenge excess H2O2, but also act as regulatory proteins, play an active role in redox signaling, and maintain mitochondrial membrane integrity. Overexpression of MAO-A is associated with increased oxidative damage, leading to mitochondrial dysfunction and subsequent progression of cardiovascular diseases (CVD), including ischemia/reperfusion injury and heart failure. Considering the central role of oxidative damage in the pathogenesis of many CVD, targeting PRDXs activation and MAO-A inhibition may offer new therapeutic strategies aimed at improving cardiac function under conditions of pathological load related to oxidative damage. Keywords: Mitochondria, Peroxiredoxin, Monoamine oxidase-A, Reactive oxygen species, Cardioprotective signaling.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 6","pages":"887-900"},"PeriodicalIF":1.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11835206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Influence of micro- and nanoplastics on mitochondrial function in the cardiovascular system: a review of the current literature. 微塑料和纳米塑料对心血管系统线粒体功能的影响:当前文献综述。
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935500
T Lerchner, J Jedlička, M Kripnerová, J Dejmek, J Kuncová

Mitochondria represent pivotal cellular organelles endowed with multifaceted functionalities encompassing cellular respiration, metabolic processes, calcium turnover, and the regulation of apoptosis, primarily through the generation of reactive oxygen species (ROS). Perturbations in mitochondrial dynamics have been intricately linked to the etiology of numerous cardiovascular pathologies, such as heart failure, ischemic heart disease, and various cardiomyopathies. Notably, recent attention has been directed towards the detrimental impact of micro- and nanoplastic pollution on mitochondrial integrity, an area underscored by a paucity of comprehensive investigations. Given the escalating prevalence of plastic particle contamination and the concomitant burden of cardiovascular disease in aging populations, understanding the interplay between mitochondria within the cardiovascular system and micro- and nanoplastic pollution assumes paramount importance. This review endeavors to elucidate the current albeit limited comprehension surrounding this complex interplay. Key words Mitochondria, Nanoplastics, Microplastics, Cardiovascular system, Endothelial function, Oxidative phosphorylation.

线粒体是关键的细胞器,具有多方面的功能,包括细胞呼吸、代谢过程、钙转换和细胞凋亡的调节,主要通过产生活性氧(ROS)。线粒体动力学的扰动与许多心血管疾病(如心力衰竭、缺血性心脏病和各种心肌病)的病因有着复杂的联系。值得注意的是,最近的注意力集中在微和纳米塑料污染对线粒体完整性的有害影响上,这一领域缺乏全面的研究。鉴于塑料颗粒污染的日益普遍,以及老龄化人群中心血管疾病的伴随负担,了解心血管系统内线粒体与微纳米塑料污染之间的相互作用具有至关重要的意义。这篇综述试图阐明目前对这种复杂相互作用的理解,尽管理解有限。关键词线粒体,纳米塑料,微塑料,心血管系统,内皮功能,氧化磷酸化
{"title":"Influence of micro- and nanoplastics on mitochondrial function in the cardiovascular system: a review of the current literature.","authors":"T Lerchner, J Jedlička, M Kripnerová, J Dejmek, J Kuncová","doi":"10.33549/physiolres.935500","DOIUrl":"10.33549/physiolres.935500","url":null,"abstract":"<p><p>Mitochondria represent pivotal cellular organelles endowed with multifaceted functionalities encompassing cellular respiration, metabolic processes, calcium turnover, and the regulation of apoptosis, primarily through the generation of reactive oxygen species (ROS). Perturbations in mitochondrial dynamics have been intricately linked to the etiology of numerous cardiovascular pathologies, such as heart failure, ischemic heart disease, and various cardiomyopathies. Notably, recent attention has been directed towards the detrimental impact of micro- and nanoplastic pollution on mitochondrial integrity, an area underscored by a paucity of comprehensive investigations. Given the escalating prevalence of plastic particle contamination and the concomitant burden of cardiovascular disease in aging populations, understanding the interplay between mitochondria within the cardiovascular system and micro- and nanoplastic pollution assumes paramount importance. This review endeavors to elucidate the current albeit limited comprehension surrounding this complex interplay. Key words Mitochondria, Nanoplastics, Microplastics, Cardiovascular system, Endothelial function, Oxidative phosphorylation.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 S3","pages":"S685-S695"},"PeriodicalIF":1.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
New possibilities of the prevention and treatment of cardiovascular pathologies. the potential of molecular hydrogen in the reduction of oxidative stress and its consequences. 预防和治疗心血管疾病的新可能性。氢分子在减少氧化应激中的潜力及其后果。
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31 DOI: 10.33549/physiolres.935491
J Slezák, T Ravingerová, B Kura

Disproportion between reactive oxygen species (ROS) production and the body's antioxidant system can cause oxidative stress, which is considered a common denominator in various pathological conditions, including cardiovascular diseases, aging, and cognitive disorders. The generation of free radicals, which occurs through partial reduction of oxygen, can quickly overwhelm the endogenous antioxidant system capacity of the cell. This causes lipid, protein, DNA and RNA damage, inflammation, and overall cell degeneration, which can be mitigated by various antioxidants. However, their use in human medicine did not bring the expected effect. Molecular hydrogen (H2), due to its unique physical and chemical properties, provides a number of benefits for alleviating oxidative stress. H2 is superior to conventional antioxidants as it can selectively reduce (.)OH radicals while preserving important ROS that are otherwise used for normal cell signaling. Key words Oxidative stress, Cardiovascular diseases, Molecular hydrogen, ROS, Inflammation.

活性氧(ROS)的产生与身体的抗氧化系统之间的失衡会导致氧化应激,这被认为是各种病理状况的共同特征,包括心血管疾病、衰老和认知障碍。自由基的产生,发生在部分氧的减少,可以迅速压倒细胞的内源性抗氧化系统的能力。这会导致脂质、蛋白质、DNA和RNA损伤、炎症和整体细胞退化,这些都可以通过各种抗氧化剂来缓解。然而,它们在人体医学中的应用并没有带来预期的效果。分子氢(H2)由于其独特的物理和化学性质,为减轻氧化应激提供了许多好处。H2优于常规抗氧化剂,因为它可以选择性地还原(。OH自由基同时保留了用于正常细胞信号传递的重要ROS。【关键词】氧化应激,心血管疾病,分子氢,ROS,炎症
{"title":"New possibilities of the prevention and treatment of cardiovascular pathologies. the potential of molecular hydrogen in the reduction of oxidative stress and its consequences.","authors":"J Slezák, T Ravingerová, B Kura","doi":"10.33549/physiolres.935491","DOIUrl":"10.33549/physiolres.935491","url":null,"abstract":"<p><p>Disproportion between reactive oxygen species (ROS) production and the body's antioxidant system can cause oxidative stress, which is considered a common denominator in various pathological conditions, including cardiovascular diseases, aging, and cognitive disorders. The generation of free radicals, which occurs through partial reduction of oxygen, can quickly overwhelm the endogenous antioxidant system capacity of the cell. This causes lipid, protein, DNA and RNA damage, inflammation, and overall cell degeneration, which can be mitigated by various antioxidants. However, their use in human medicine did not bring the expected effect. Molecular hydrogen (H2), due to its unique physical and chemical properties, provides a number of benefits for alleviating oxidative stress. H2 is superior to conventional antioxidants as it can selectively reduce (.)OH radicals while preserving important ROS that are otherwise used for normal cell signaling. Key words Oxidative stress, Cardiovascular diseases, Molecular hydrogen, ROS, Inflammation.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 S3","pages":"S671-S684"},"PeriodicalIF":1.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
LDHA- Mediated Histone Lactylation Promotes the Nonalcoholic Fatty Liver Disease Progression Through Targeting The METTL3/ YTHDF1/SCD1 m6A Axis.
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31
J Meng, C Yan, J Liu

Nonalcoholic fatty liver disease (NAFLD) is characterized by elevated hepatic lipids caused by nonalcoholic factors, where histone lactylation is lately discovered as a modification driving disease progression. This research aimed to explore the role of histone 3 lysine 18 lactylation (H3K18lac) in NAFLD progression using a high-fat diet (HFD)-treated mouse model and free fatty acids (FFA)-treated L-02 cell lines. Lipids accumulation was screened via Oil Red O staining, real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, and commercially available kits. Similarly, molecular mechanism was analyzed using immunoprecipitation (IP), dual-luciferase reporter assay, and RNA decay assay. Results indicated that FFA upregulated lactate dehydrogenase A (LDHA) and H3K18lac levels in L-02 cells. Besides, LDHA-mediated H3K18lac was enriched on the proximal promoter of methyltransferase 3 (METTL3), translating into an increased expression. Moreover, METTL3 or LDHA knockdown relieved lipid accumulation, decreased total cholesterol (TC) and triglyceride (TG) levels, and downregulated lipogenesis-related proteins in FFA-treated L-02 cell lines, in addition to enhancing the m6A and mRNA levels of stearoyl-coenzyme A desaturase 1 (SCD1). The m6A modification of SCD1 was recognized by YTH N6-methyladenosine RNA binding protein F1 (YTHDF1), resulting in enhanced mRNA stability. LDHA was found to be highly expressed in HFD-treated mice, where knocking down LDHA attenuated HFD-induced hepatic steatosis. These findings demonstrated that LDHA-induced H3K18lac promoted NAFLD progression, where LDHA-induced H3K18lac in METTL3 promoter elevated METTL3 expression, thereby promoting m6A methylation and stabilizing SCD1 via a YTHDF1-dependent manner. Keywords: Nonalcoholic fatty liver disease, LDHA, METTL3, YTHDF1, Histone lactylation.

{"title":"LDHA- Mediated Histone Lactylation Promotes the Nonalcoholic Fatty Liver Disease Progression Through Targeting The METTL3/ YTHDF1/SCD1 m6A Axis.","authors":"J Meng, C Yan, J Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD) is characterized by elevated hepatic lipids caused by nonalcoholic factors, where histone lactylation is lately discovered as a modification driving disease progression. This research aimed to explore the role of histone 3 lysine 18 lactylation (H3K18lac) in NAFLD progression using a high-fat diet (HFD)-treated mouse model and free fatty acids (FFA)-treated L-02 cell lines. Lipids accumulation was screened via Oil Red O staining, real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, and commercially available kits. Similarly, molecular mechanism was analyzed using immunoprecipitation (IP), dual-luciferase reporter assay, and RNA decay assay. Results indicated that FFA upregulated lactate dehydrogenase A (LDHA) and H3K18lac levels in L-02 cells. Besides, LDHA-mediated H3K18lac was enriched on the proximal promoter of methyltransferase 3 (METTL3), translating into an increased expression. Moreover, METTL3 or LDHA knockdown relieved lipid accumulation, decreased total cholesterol (TC) and triglyceride (TG) levels, and downregulated lipogenesis-related proteins in FFA-treated L-02 cell lines, in addition to enhancing the m6A and mRNA levels of stearoyl-coenzyme A desaturase 1 (SCD1). The m6A modification of SCD1 was recognized by YTH N6-methyladenosine RNA binding protein F1 (YTHDF1), resulting in enhanced mRNA stability. LDHA was found to be highly expressed in HFD-treated mice, where knocking down LDHA attenuated HFD-induced hepatic steatosis. These findings demonstrated that LDHA-induced H3K18lac promoted NAFLD progression, where LDHA-induced H3K18lac in METTL3 promoter elevated METTL3 expression, thereby promoting m6A methylation and stabilizing SCD1 via a YTHDF1-dependent manner. Keywords: Nonalcoholic fatty liver disease, LDHA, METTL3, YTHDF1, Histone lactylation.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 6","pages":"985-999"},"PeriodicalIF":1.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11835221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension.
IF 1.9 4区 医学 Q3 PHYSIOLOGY Pub Date : 2024-12-31
J Zicha, I Vaněčková

Sympathetic hyperactivity and relative NO deficiency are characteristic alterations in both genetic and salt hypertension. The contribution of these abnormalities to blood pressure (BP) maintenance can be determined in conscious rats using a consecutive blockade of particular vasoactive systems. Thus, the contribution of pressor effects of angiotensin II to the maintenance of high BP is usually small, but the role of renin-angiotensin system in the development of hypertension mediated by central and peripheral effects of angiotensin II on sympathetic activity is highly important. This is even true in angiotensin-dependent hypertension of heterozygous Ren-2 transgenic rats in which sympathetic hyperactivity is increasing with age. Central sympathoexcitation in this hypertensive model can be inhibited by lower losartan doses than peripheral angiotensin II-dependent vasoconstriction. This experimental model also yielded important knowledge on nephroprotective effects of new therapeutic drugs - endothelin receptor type A blockers. A considerable part of sympathetic vasoconstriction is dependent on the interaction of Ca2+ sensitization (RhoA/Rho kinase pathway) and Ca2+ influx (through L-VDCC). The blockade of these pathways prevents a major part of sympathetic vasoconstriction. Ca2+ sensitization seems to be attenuated in genetic hypertension in order to compensate increased Ca2+ influx. In contrast, enhanced Ca2+ sensitization is a hallmark of salt sensitivity in Dahl rats in which salt hypertension is dependent on increased Ca2+ influx. The attention should also be paid to the impairment of arterial baroreflex sensitivity which permits enhanced BP responses to pressor or depressor stimuli. Some abnormalities can be studied in blood vessels isolated from hypertensive rats but neither conduit arteries nor mesenteric resistance arteries represent the vascular beds decisive for the increased peripheral resistance and high BP. Keywords: Sympathetic vasoconstriction, NO-dependent vasodilatation, Calcium sensitization, Calcium influx, Arterial baroreflex, Spontaneously hypertensive rats, Salt hypertensive Dahl rats, Ren-2 transgenic rats, RAS blockade, SNS blockade, NOS inhibition, Endothelin, Vascular contraction and relaxation, Isolated conduit and resistance arteries, EDCF, PGI2, BKCa channels.

{"title":"Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension.","authors":"J Zicha, I Vaněčková","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Sympathetic hyperactivity and relative NO deficiency are characteristic alterations in both genetic and salt hypertension. The contribution of these abnormalities to blood pressure (BP) maintenance can be determined in conscious rats using a consecutive blockade of particular vasoactive systems. Thus, the contribution of pressor effects of angiotensin II to the maintenance of high BP is usually small, but the role of renin-angiotensin system in the development of hypertension mediated by central and peripheral effects of angiotensin II on sympathetic activity is highly important. This is even true in angiotensin-dependent hypertension of heterozygous Ren-2 transgenic rats in which sympathetic hyperactivity is increasing with age. Central sympathoexcitation in this hypertensive model can be inhibited by lower losartan doses than peripheral angiotensin II-dependent vasoconstriction. This experimental model also yielded important knowledge on nephroprotective effects of new therapeutic drugs - endothelin receptor type A blockers. A considerable part of sympathetic vasoconstriction is dependent on the interaction of Ca2+ sensitization (RhoA/Rho kinase pathway) and Ca2+ influx (through L-VDCC). The blockade of these pathways prevents a major part of sympathetic vasoconstriction. Ca2+ sensitization seems to be attenuated in genetic hypertension in order to compensate increased Ca2+ influx. In contrast, enhanced Ca2+ sensitization is a hallmark of salt sensitivity in Dahl rats in which salt hypertension is dependent on increased Ca2+ influx. The attention should also be paid to the impairment of arterial baroreflex sensitivity which permits enhanced BP responses to pressor or depressor stimuli. Some abnormalities can be studied in blood vessels isolated from hypertensive rats but neither conduit arteries nor mesenteric resistance arteries represent the vascular beds decisive for the increased peripheral resistance and high BP. Keywords: Sympathetic vasoconstriction, NO-dependent vasodilatation, Calcium sensitization, Calcium influx, Arterial baroreflex, Spontaneously hypertensive rats, Salt hypertensive Dahl rats, Ren-2 transgenic rats, RAS blockade, SNS blockade, NOS inhibition, Endothelin, Vascular contraction and relaxation, Isolated conduit and resistance arteries, EDCF, PGI2, BKCa channels.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 6","pages":"901-928"},"PeriodicalIF":1.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11835210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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