Jin Kaiqin, Ma Zijun, Wang Xiaohe, Gong Chen, Sheng Jianlong, Chen Jun, Shen Shichun
Department of Cardiology, Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), Hubei University of Medicine, 442000 Shiyan, Hubei, China.
Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), Hubei University of Medicine, 442000 Shiyan, Hubei, China.
Rev Cardiovasc Med. 2024 Nov 21;25(11):419. doi: 10.31083/j.rcm2511419. eCollection 2024 Nov.
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.
根据目前的统计数据，心血管疾病的死亡率仍然很高，冠状动脉疾病是主要死因。尽管近年来经皮冠状动脉介入治疗（PCI）已广泛应用，使心肌梗死（MI）的死亡率显著下降，但心肌梗死后的病理性心脏重塑和心力衰竭仍然构成重大的临床挑战。心肌缺血再灌注（MIR）损伤是一个复杂的病理生理过程，巨噬细胞在这种损伤中的作用一直是重要的研究焦点。MIR后，巨噬细胞浸润，吞噬组织碎片和坏死细胞，并分泌促炎因子。这种初始反应对于清除受损组织至关重要。随后，促炎巨噬细胞（M1）转变为抗炎表型（M2），这种转变对于心肌纤维化和心脏重塑至关重要。这个过程是动态、复杂且持续的。为了增进对这一过程的理解，本综述阐述了心脏内巨噬细胞的分类和功能，涵盖了近期关于心肌梗死后通过后续MIR损伤和纤维化所涉及的信号通路的研究。最终目的是减少MIR损伤，为心脏恢复营造有利环境，并改善MI患者的临床结局。
