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Role of voltage-gated potassium channel α subunits in cardiovascular system. 电压门控钾通道 α 亚基在心血管系统中的作用
生理学报 Pub Date : 2024-10-25
Jin-Ru Yang, Peng Huang, Shu-Kuan Ling
{"title":"Role of voltage-gated potassium channel α subunits in cardiovascular system.","authors":"Jin-Ru Yang, Peng Huang, Shu-Kuan Ling","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Voltage-gated ion channels (VGICs) are central to cellular excitation, orchestrating skeletal and cardiac muscle contractions and enabling neural signal transduction. Among these, voltage-gated potassium (Kv) channels are particularly significant in cardiac electrophysiology, especially during the repolarization phase of the cardiac action potential. In cardiac myocytes, Kv channels are integral to a multitude of sophisticated functions, including electrical conduction. Despite their importance, research on Kv channels in the context of cardiovascular diseases is limited. This review offers a comprehensive summary of the structural complexities of Kv channels, delineating the regulatory mechanisms involved in channel gating, expression, and membrane localization. Additionally, we examine the role of different Kv α-subunits in modulating Kv channels and their impact on cardiac remodeling, and assess the potential of targeting Kv channels for the development of anti-arrhythmic therapies.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"761-774"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520695","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
[Exogenous EPO protects HT22 cells from intermittent hypoxia-induced injury by activating JAK2-STAT5 signaling pathway]. [外源性 EPO 通过激活 JAK2-STAT5 信号通路保护 HT22 细胞免受间歇性缺氧诱导的损伤】。］
生理学报 Pub Date : 2024-10-25
Ke-Rong Qi, Xue Chen, Jian-Chao Si, Qing-Qing Liu, Sheng-Chang Yang
{"title":"[Exogenous EPO protects HT22 cells from intermittent hypoxia-induced injury by activating JAK2-STAT5 signaling pathway].","authors":"Ke-Rong Qi, Xue Chen, Jian-Chao Si, Qing-Qing Liu, Sheng-Chang Yang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aim of this study was to investigate the effects of exogenous erythropoietin (EPO) on intermittent hypoxia (IH)-induced neuronal injury and the underlying mechanism. Mouse hippocampal neuron HT22 cells were exposed to IH for different durations (1% O<sub>2</sub> for 7 min/21% O<sub>2</sub> for 3 min, one cycle for 10 min). Cell viability was detected by CCK-8. EPO content in the supernatant of cell culture medium was detected by ELISA kit, and the protein expression was detected by Western blot. EPO receptor (EPOR) protein expression was detected by immunofluorescence staining and Western blot. Cellular apoptosis and mitochondrial membrane potential were detected by the corresponding kits. Reactive oxygen species (ROS) level was detected by DCFH probe, and expression levels of JAK2-STAT5 signaling pathway-related proteins were detected by Western blot. The results showed that IH exposure significantly decreased HT22 cell activity. EPO and EPOR protein expressions were significantly up-regulated at 12 h of IH exposure, but down-regulated at 24 and 48 h. In IH-treated HT22 cells, exogenous EPO significantly increased cell activity and mitochondrial membrane potential, decreased ROS levels and cell apoptosis, up-regulated Nrf-2 and heme oxygenase 1 (HO-1) protein expression levels, decreased Cleaved-Caspase-3/Caspase-3 and Bax/Bcl-2 ratios, and promoted the phosphorylation of JAK2-STAT5 pathway-related proteins. Whereas JAK2 and STAT5 blockers both reversed these neuronal protective effects of EPO. These results suggest exogenous EPO inhibits IH-induced oxidative stress and apoptosis by activating the JAK2-STAT5 signaling pathway, thus exerting a neuronal protective effect.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"691-702"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520679","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
[Research progress on the mechanism of autophagy flow injury caused by lysosomal dysfunction after cerebral ischemia]. [脑缺血后溶酶体功能障碍导致自噬流损伤机制的研究进展]。
生理学报 Pub Date : 2024-10-25
Jia-Qian Wang, Hong-Yun He, Yi-Hao Deng
{"title":"[Research progress on the mechanism of autophagy flow injury caused by lysosomal dysfunction after cerebral ischemia].","authors":"Jia-Qian Wang, Hong-Yun He, Yi-Hao Deng","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Ischemic stroke is an acute cerebrovascular disease caused by cerebral vascular obstruction, which is the third leading cause of human death and disability. Multiple studies have demonstrated that autophagy plays a positive role in neurons after ischemic stroke. Autophagy is the main intracellular mechanism that mediates the degradation and recycling of various substrates in lysosomes, so it is very important to maintain normal function of lysosomes. However, cerebral ischemia can result in significant impairment of lysosomal function, subsequently leading to disruption in autophagy flow and exacerbation of neuronal injury. This review elucidates the mechanism of autophagic flux injury resulting from lysosomal dysfunction induced by impaired fusion between autophagosomes and lysosomes, alterations in the acidic environment within lysosomes, and diminished biosynthesis of lysosomes following ischemic stroke. The lysosome is regarded as the primary focal point for investigating the mechanism of autophagic flux injury, with the aim of modulating neuronal autophagic flux to improve cerebral ischemia-induced brain injury. This approach holds potential for exerting a neuroprotective effect and providing a novel avenue for stroke treatment.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"783-790"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520686","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 role of the tryptophan-kynurenine pathway in neuropathic pain]. [色氨酸-犬尿氨酸途径在神经性疼痛中的作用]。
生理学报 Pub Date : 2024-10-25
Zi-Han Wu, Hao-Jun You, Jing Lei
{"title":"[The role of the tryptophan-kynurenine pathway in neuropathic pain].","authors":"Zi-Han Wu, Hao-Jun You, Jing Lei","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The kynurenine pathway (KP) is the main metabolic pathway of tryptophan in the diet. Existing research has shown that KP plays a key role in the pathogenesis of various diseases. It has been demonstrated that kynurenine metabolic enzymes, such as indoleamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO), are involved in various types of pain, particularly the occurrence and development of neuropathic pain. This article reviewed the role of KP, metabolites and enzymes, as well as the analgesic effects and mechanisms of KP in neuropathic pain, providing reference for the application of KP in the basic research and clinical treatment of neuropathic pain.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 5","pages":"818-826"},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520692","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
[Molecular mechanism of CDO1 regulating common metabolic diseases]. [CDO1调控常见代谢性疾病的分子机制]。
Acta physiologica Sinica Pub Date : 2024-08-25
Qi Liu, Wen-Qing Shen
{"title":"[Molecular mechanism of CDO1 regulating common metabolic diseases].","authors":"Qi Liu, Wen-Qing Shen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cysteine dioxygenase type 1 (CDO1) belongs to the cysteine dioxygenase (CDO) family. CDO1 is the key enzyme in cysteine catabolism and taurine synthesis. CDO1 is highly expressed in liver, adipose tissue, pancreas, kidney, lung, brain and small intestine. CDO1 is involved in the pathophysiological regulation of various common metabolic diseases, such as lipid metabolism disorders, insulin resistance, obesity, tumors/cancers, and neurodegenerative diseases. This article summarizes the research progress on the molecular mechanisms of CDO1 regulation of common metabolic diseases in recent years, aiming to provide new theoretical and practical basis for CDO1-targeted therapy for insulin resistance, obesity, tumors/cancers, and neurodegenerative diseases.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"576-586"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078750","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 effect of exercise on platelet-activating factor metabolism in the livers of rats fed high-fat diet]. [运动对高脂饮食大鼠肝脏中血小板活化因子代谢的影响]。
Acta physiologica Sinica Pub Date : 2024-08-25
Shang-Yan Dong, Wei Li, Li-Feng Wang, Zhen-Mao Lin, Ming-Jian Chen, Ting Li
{"title":"[The effect of exercise on platelet-activating factor metabolism in the livers of rats fed high-fat diet].","authors":"Shang-Yan Dong, Wei Li, Li-Feng Wang, Zhen-Mao Lin, Ming-Jian Chen, Ting Li","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This paper aimed to investigate the effects of exercise on hepatic platelet-activating factor (PAF) metabolism in rats fed a high-fat diet. Thirty-two male Sprague-Dawley (SD) rats were divided into control group (C), high-fat diet group (H), exercise group (EC), and high-fat diet+exercise group (EH). Serum lipids, glucose, insulin and markers of hepatic injury after a 16-week dietary and/or exercise intervention (60 min/day, 6 times/week) were measured by biochemical analysis; liver lipidomic profiles were analyzed by liquid chromatograph-mass spectrometer (LC-MS). Gene and protein expression of enzymes related to PAF metabolism were determined by qPCR and Western blot respectively. The results showed that high-fat diet feeding significantly increased the levels of low-density lipoprotein-cholesterol (LDL-C) and liver injury markers including purine nucleoside phosphorylase (PNP) and malondialdehyde (MDA) in rats, which were decreased by exercise. Furthermore, high-fat diet feeding significantly increased the hepatic PAF content, which was also attenuated by exercise. In addition, although high-fat diet treatment resulted in an increase in the expression of both PAF synthetase (PAF-CPT and PLA2) and hydrolase (Lp-PLA2 and PAF-AH(II)), induction of PAF synthetase was much greater than that of PAF hydrolase. While exercise increased the expression of Lp-PLA2 and PAF-AH(II) and decreased the expression of PAF-CPT and PLA2, key PAF synthesizing enzymes. In conclusion, high-fat diet-induced increase in hepatic PAF content is mainly due to the increase of its pathological synthesis at the translational level. Exercise reduces hepatic PAF content in high-fat fed rats by increasing PAF hydrolysis and decreasing its synthesis.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"537-546"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078816","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
[Effects of stress on the structure and function of microglia]. [压力对小胶质细胞结构和功能的影响]。
Acta physiologica Sinica Pub Date : 2024-08-25
Yu Xiao, Li-Jie Liu
{"title":"[Effects of stress on the structure and function of microglia].","authors":"Yu Xiao, Li-Jie Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The activation of stressors can disrupt the body's homeostasis, leading to the release of stress hormones such as epinephrine, noradrenaline, and glucocorticoids. Moreover, emerging evidence highlights the profound impact of stress on microglia, which are specialized macrophages residing in the brain's parenchyma. Following stress, microglia exhibit notable morphological activation and increased phagocytic activity. Microglia express various receptors that enable them to respond to stress hormones originating from both central and peripheral sources, thereby exerting pro-inflammatory or anti-inflammatory effects. In this article, we review the advancements in studying the structural and functional changes of microglia induced by exposure to stressors. Additionally, we explore the role of stress hormones in mediating the effects of these stressors on microglia.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"663-671"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078747","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
[Research progress on mitochondrial copper homeostasis imbalance and fibrosis diseases]. [线粒体铜平衡失调与纤维化疾病的研究进展]。
Acta physiologica Sinica Pub Date : 2024-08-25
Sai-Ya Zhu, Jing Liu, Chen Yu
{"title":"[Research progress on mitochondrial copper homeostasis imbalance and fibrosis diseases].","authors":"Sai-Ya Zhu, Jing Liu, Chen Yu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Copper ions serve as co-factors for various enzymes and participate in multiple cellular processes. Mitochondria are essential copper reservoirs within the cell. Previous reviews have extensively summarized the association between mitochondrial copper homeostasis imbalance and hematologic disorders, cardiomyopathies, and skeletal myopathies. However, there is limited information regarding its association with organ fibrosis. This article outlines the role and mechanism of disrupted mitochondrial copper homeostasis in fibrotic diseases, and systematically elaborates copper absorption and transport, as well as the regulation of copper homeostasis within mitochondria. It focuses on the impacts of mitochondrial copper overload and deficiency on fibrotic diseases, and the application of copper chelators as potential anti-fibrotic therapeutic approaches.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"597-604"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078813","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
[Research progress on eosinophil heterogeneity in asthma]. [哮喘中嗜酸性粒细胞异质性的研究进展]。
Acta physiologica Sinica Pub Date : 2024-08-25
Yan Chen, Song-Min Ying, Chao Zhang
{"title":"[Research progress on eosinophil heterogeneity in asthma].","authors":"Yan Chen, Song-Min Ying, Chao Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Asthma is a heterogeneous disease characterized by chronic airway inflammation. More than half of asthma cases are induced by allergens. Eosinophils accumulate in large numbers in the airways, and their number is closely related to the severity of asthma. In recent years, extensive research has been conducted on the pathogenesis of eosinophils in asthma and the targeted therapeutic drugs for them. This article mainly reviews the research progress on the important role of eosinophil heterogeneity in the occurrence and development of asthma, and provides ideas for the personalized and precise treatment of asthma in the future.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"643-652"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078812","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
[Progress on the effects of cancer-related fibroblast induced by Helicobacter pylori infection on gastric epithelial-mesenchymal transition]. [幽门螺杆菌感染诱导的癌症相关成纤维细胞对胃上皮-间质转化影响的研究进展]。
Acta physiologica Sinica Pub Date : 2024-08-25
Yi-Lin Li, Li-Fei Zheng
{"title":"[Progress on the effects of cancer-related fibroblast induced by Helicobacter pylori infection on gastric epithelial-mesenchymal transition].","authors":"Yi-Lin Li, Li-Fei Zheng","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Helicobacter pylori (Hp) is a Gram-negative bacterium that colonizes in the gastric mucosa. Hp induces the production of cancer-associated fibroblasts (CAF) in the stomach. The virulence factors of Hp and CAF trigger epithelial-mesenchymal transition (EMT), leading to local inflammation, damage to the gastric mucosa, and the occurrence of chronic gastritis. Here, we summarize the molecular mechanisms of CAF mediated gastric EMT after Hp infection, providing new insights into potential molecular targets and strategies for the future treatment of Hp infection associated gastric cancer.</p>","PeriodicalId":7134,"journal":{"name":"Acta physiologica Sinica","volume":"76 4","pages":"547-560"},"PeriodicalIF":0.0,"publicationDate":"2024-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078809","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
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