{"title":"The Role of Cardiac Macrophages in Inflammation and Fibrosis after Myocardial Ischemia-Reperfusion.","authors":"Kaiqin Jin, Zijun Ma, Xiaohe Wang, Chen Gong, Jianlong Sheng, Jun Chen, Shichun Shen","doi":"10.31083/j.rcm2511419","DOIUrl":null,"url":null,"abstract":"<p><p>According to current statistics, the mortality rate of cardiovascular diseases remains high, with coronary artery disease being the primary cause of death. Despite the widespread adoption of percutaneous coronary intervention (PCI) in recent years, which has led to a notable decrease in the mortality rate of myocardial infarction (MI), the pathological cardiac remodeling and heart failure that follow myocardial infarction still pose significant clinical challenges. Myocardial ischemia-reperfusion (MIR) injury represents a complex pathophysiological process, and the involvement of macrophages in this injury has consistently been a subject of significant focus. Following MIR, macrophages infiltrate, engulfing tissue debris and necrotic cells, and secreting pro-inflammatory factors. This initial response is crucial for clearing damaged tissue. Subsequently, the pro-inflammatory macrophages (M1) transition to an anti-inflammatory phenotype (M2), a shift that is essential for myocardial fibrosis and cardiac remodeling. This process is dynamic, complex, and continuous. To enhance understanding of this process, this review elaborates on the classification and functions of macrophages within the heart, covering recent research on signaling pathways involved in myocardial infarction through subsequent MIR injury and fibrosis. The ultimate aim is to reduce MIR injury, foster a conducive environment for cardiac recovery, and improve clinical outcomes for MI patients.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"25 11","pages":"419"},"PeriodicalIF":1.9000,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11607502/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Reviews in cardiovascular medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.31083/j.rcm2511419","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
According to current statistics, the mortality rate of cardiovascular diseases remains high, with coronary artery disease being the primary cause of death. Despite the widespread adoption of percutaneous coronary intervention (PCI) in recent years, which has led to a notable decrease in the mortality rate of myocardial infarction (MI), the pathological cardiac remodeling and heart failure that follow myocardial infarction still pose significant clinical challenges. Myocardial ischemia-reperfusion (MIR) injury represents a complex pathophysiological process, and the involvement of macrophages in this injury has consistently been a subject of significant focus. Following MIR, macrophages infiltrate, engulfing tissue debris and necrotic cells, and secreting pro-inflammatory factors. This initial response is crucial for clearing damaged tissue. Subsequently, the pro-inflammatory macrophages (M1) transition to an anti-inflammatory phenotype (M2), a shift that is essential for myocardial fibrosis and cardiac remodeling. This process is dynamic, complex, and continuous. To enhance understanding of this process, this review elaborates on the classification and functions of macrophages within the heart, covering recent research on signaling pathways involved in myocardial infarction through subsequent MIR injury and fibrosis. The ultimate aim is to reduce MIR injury, foster a conducive environment for cardiac recovery, and improve clinical outcomes for MI patients.
期刊介绍:
RCM is an international, peer-reviewed, open access journal. RCM publishes research articles, review papers and short communications on cardiovascular medicine as well as research on cardiovascular disease. We aim to provide a forum for publishing papers which explore the pathogenesis and promote the progression of cardiac and vascular diseases. We also seek to establish an interdisciplinary platform, focusing on translational issues, to facilitate the advancement of research, clinical treatment and diagnostic procedures. Heart surgery, cardiovascular imaging, risk factors and various clinical cardiac & vascular research will be considered.