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[Research progress on chronic intermittent hypoxia and cognitive impairment]. [慢性间歇性缺氧与认知障碍的研究进展]。
生理学报 Pub Date : 2024-10-25
Ke-Rong Qi, Xue Chen, Jian-Chao Si, Sheng-Chang Yang
{"title":"[Research progress on chronic intermittent hypoxia and cognitive impairment].","authors":"Ke-Rong Qi, Xue Chen, Jian-Chao Si, Sheng-Chang Yang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Obstructive sleep apnea (OSA) affects quality of life and health in nearly 1 billion patients all over the world. With aging society, OSA increases the risk of Alzheimer's disease and leads to severe cognitive impairment. Chronic intermittent hypoxia (CIH), the core pathological mechanism of OSA, may induce synaptic plasticity damage and cognitive impairment, and decrease learning and memory and attention ability. However, the molecular mechanism underlying OSA is still not fully understood. And, there is no targeted treatment strategy for cognitive impairment in patients with OSA. Firstly, the correlation between OSA and cognitive dysfunction was summarized in this review. Secondly, the molecular mechanism of CIH-induced cognitive impairment was elucidated from the perspectives of synaptic plasticity damage, oxidative stress, inflammation, endoplasmic reticulum stress, apoptosis, mitochondrial dysfunction and autophagy. Finally, the current treatment strategy for cognitive impairment in patients with OSA was summarized.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520684","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 oligodendrocyte precursor cells in immunoregulation]. [少突胶质前体细胞在免疫调节中的作用]。
生理学报 Pub Date : 2024-10-25
Xiang Chen, Cheng He, Peng Liu
{"title":"[The role of oligodendrocyte precursor cells in immunoregulation].","authors":"Xiang Chen, Cheng He, Peng Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Oligodendrocyte precursor cells (OPCs) are recognized as the progenitors responsible for the generation of oligodendrocytes, which play a critical role in myelination of central nervous system. In addition, in demyelinating diseases, such as brain trauma, ischemia, and multiple sclerosis, OPCs are also found in demyelinated regions, but fail to differentiate into mature oligodendrocytes and remyelinate. From traditional view, OPC is victim of immune response. However, recent studies have shed light on immune associated OPCs (imOPCs), which are induced by interferon γ (IFN-γ), and interleukin 17 (IL-17), and are involved in the innate and adaptive immune activation. By expressing multiple natural immune pattern recognition receptors, such as Toll-like receptors, imOPCs can phagocytose myelin debris for antigen presentation. Furthermore, imOPCs can also secrete various inflammatory and chemotactic factors to regulate the differentiation of Th0 cells and the recruitment of NK cells, granulocytes and macrophages. Thus, it is of great importance to explore the immunoregulatory function of OPCs to elucidate the mechanisms and treatments of demyelinating diseases.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520691","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 of the effects of high-intensity interval training on excess post-exercise oxygen consumption in human]. [高强度间歇训练对人体运动后多余耗氧量影响的研究进展]。
生理学报 Pub Date : 2024-10-25
Yang-Yang Su, Xiao-Ning Dong, Xiu-Qin Wu
{"title":"[Research progress of the effects of high-intensity interval training on excess post-exercise oxygen consumption in human].","authors":"Yang-Yang Su, Xiao-Ning Dong, Xiu-Qin Wu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Elevated human metabolism during recovery is associated with increased excess post-exercise oxygen consumption (EPOC). EPOC is linearly related to exercise duration and exponentially related to exercise intensity. It is commonly believed that near-maximal intensity interval training prompts the body to produce greater EPOC. This review focuses on the origin and development of high-intensity interval training (HIIT), analyzes its concept, classification and function, and discusses its effects on human EPOC. HIIT promotes a significant increase in EPOC during the fast recovery period, whereas the changes of EPOC during the slow recovery period are still inconclusive; Sprint interval training (SIT) promotes a significant increase in EPOC throughout the whole recovery period. Compared with HIIT, the body's energy expenditure and oxygen uptake (VO<sub>2</sub>) increase significantly during moderate-intensity continuous training (MICT), but the total energy expenditure and VO<sub>2</sub> during exercise and 24 h of recovery period are similar between the two types of exercises, indicating that greater EPOC is generated during the recovery period of HIIT. The mechanisms by which interval training improves EPOC include increasing lung ventilation and catecholamine secretion, accelerating systemic circulation, increasing body temperature, promoting glycogen resynthesis, rapid recruitment of fast twitch muscle fibers and uncoupling of mitochondrial respiration, up-regulating hypoxia inducible factor-1 alpha and skeletal muscle protein, as well as improving intestinal flora.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520683","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
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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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
[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":null,"pages":null},"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":null,"pages":null},"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
[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":null,"pages":null},"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
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