Pub Date : 2023-01-01DOI: 10.2174/1570161121666230106153857
Jing Yang, Shuling Rong
Cardiovascular diseases (CVDs) based on atherosclerosis remain the main reason for death in Western countries and China. Cardiovascular research has demonstrated that its pathogenesis is closely associated with endothelial cell (EC) injury, the phenotypic transformation of vascular smooth muscle cells (VSMCs), and the abnormal biological behaviour of macrophages. In recent years, circular RNAs (circRNAs) have received much attention for their unique role in the pathogenesis of atherosclerosis. In this review, we discussed the mechanisms associated with ECs, VSMCs, and macrophages in atherosclerosis and summarized the role of circRNAs in atherosclerosis. This review aims to provide a basis for the prevention and treatment of atherosclerosis.
{"title":"The Emerging Role of CircRNAs in Atherosclerosis.","authors":"Jing Yang, Shuling Rong","doi":"10.2174/1570161121666230106153857","DOIUrl":"https://doi.org/10.2174/1570161121666230106153857","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) based on atherosclerosis remain the main reason for death in Western countries and China. Cardiovascular research has demonstrated that its pathogenesis is closely associated with endothelial cell (EC) injury, the phenotypic transformation of vascular smooth muscle cells (VSMCs), and the abnormal biological behaviour of macrophages. In recent years, circular RNAs (circRNAs) have received much attention for their unique role in the pathogenesis of atherosclerosis. In this review, we discussed the mechanisms associated with ECs, VSMCs, and macrophages in atherosclerosis and summarized the role of circRNAs in atherosclerosis. This review aims to provide a basis for the prevention and treatment of atherosclerosis.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9352021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.2174/1570161121666230315142507
Haijing Guan, Jingwen Sun, Xiuying Liang, Wenjuan Yao
Background: The pathological role of cytochrome c oxidase 5A (COX5A) in vascular neointima formation remains unknown.
Aim: This study aims to investigate the role of COX5A on platelet-derived growth factor BB (PDGFBB)- mediated smooth muscle phenotypic modulation and neointima formation and clarify the molecular mechanisms behind this effect.
Methods: For in vitro assays, human aortic vascular smooth muscle cells (HA-VSMCs) were transfected with pcDNA3.1-COX5A and COX5A siRNA to overexpress and knockdown COX5A, respectively. Mitochondrial complex IV activity, oxygen consumption rate (OCR), H2O2 and ATP production, reactive oxygen species (ROS) generation, cell proliferation, and migration were measured. For in vivo assays, rats after balloon injury (BI) were injected with recombinant lentivirus carrying the COX5A gene. Mitochondrial COX5A expression, carotid arterial morphology, mitochondrial ultrastructure, and ROS were measured.
Results: The results showed that PDGF-BB reduced the level and altered the distribution of COX5A in mitochondria, as well as reduced complex IV activity, ATP synthesis, and OCR while increasing H2O2 synthesis, ROS production, and cell proliferation and migration. These effects were reversed by overexpression of COX5A and aggravated by COX5A knockdown. In addition, COX5A overexpression attenuated BI-induced neointima formation, muscle fiber area ratio, VSMC migration to the intima, mitochondrial ultrastructural damage, and vascular ROS generation.
Conclusion: The present study demonstrated that COX5A protects VSMCs against phenotypic modulation by improving mitochondrial respiratory function and attenuating mitochondrial damage, as well as reducing oxidative stress, thereby preventing neointima formation.
{"title":"Protective Role of Cytochrome C Oxidase 5A (COX5A) against Mitochondrial Disorder and Oxidative Stress in VSMC Phenotypic Modulation and Neointima Formation.","authors":"Haijing Guan, Jingwen Sun, Xiuying Liang, Wenjuan Yao","doi":"10.2174/1570161121666230315142507","DOIUrl":"https://doi.org/10.2174/1570161121666230315142507","url":null,"abstract":"<p><strong>Background: </strong>The pathological role of cytochrome c oxidase 5A (COX5A) in vascular neointima formation remains unknown.</p><p><strong>Aim: </strong>This study aims to investigate the role of COX5A on platelet-derived growth factor BB (PDGFBB)- mediated smooth muscle phenotypic modulation and neointima formation and clarify the molecular mechanisms behind this effect.</p><p><strong>Methods: </strong>For <i>in vitro assays</i>, human aortic vascular smooth muscle cells (HA-VSMCs) were transfected with pcDNA3.1-COX5A and COX5A siRNA to overexpress and knockdown COX5A, respectively. Mitochondrial complex IV activity, oxygen consumption rate (OCR), H<sub>2</sub>O<sub>2</sub> and ATP production, reactive oxygen species (ROS) generation, cell proliferation, and migration were measured. For in vivo assays, rats after balloon injury (BI) were injected with recombinant lentivirus carrying the COX5A gene. Mitochondrial COX5A expression, carotid arterial morphology, mitochondrial ultrastructure, and ROS were measured.</p><p><strong>Results: </strong>The results showed that PDGF-BB reduced the level and altered the distribution of COX5A in mitochondria, as well as reduced complex IV activity, ATP synthesis, and OCR while increasing H<sub>2</sub>O<sub>2</sub> synthesis, ROS production, and cell proliferation and migration. These effects were reversed by overexpression of COX5A and aggravated by COX5A knockdown. In addition, COX5A overexpression attenuated BI-induced neointima formation, muscle fiber area ratio, VSMC migration to the intima, mitochondrial ultrastructural damage, and vascular ROS generation.</p><p><strong>Conclusion: </strong>The present study demonstrated that COX5A protects VSMCs against phenotypic modulation by improving mitochondrial respiratory function and attenuating mitochondrial damage, as well as reducing oxidative stress, thereby preventing neointima formation.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9751118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}