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已发表论文
急性心肌梗死中巨噬细胞极化的动态调节及其治疗潜力
Authors Xu A , Xu S, Tan X, Sun Q, Song Y, Nong Y , Wang X, Zeng Y, Fan H , Zhou Y
Received 27 May 2025
Accepted for publication 17 November 2025
Published 13 December 2025 Volume 2025:18 Pages 17363—17385
DOI https://doi.org/10.2147/JIR.S543139
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Anh Ngo
Anchen Xu,1,2 Shuai Xu,1,2 Xin Tan,1,2 Qiaoyi Sun,1,2 Yahui Song,3 Yuxin Nong,1,2 Xiangyu Wang,1,2 Yiyao Zeng,1,2 Huimin Fan,1– 3 Yafeng Zhou1,2
1Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, 215000, People’s Republic of China; 2Department of Hypertension, The Fourth Affiliated Hospital of Soochow University, Institute for Hypertension, Soochow University, Suzhou, 215000, People’s Republic of China; 3Center of Translational Medicine and Clinical Laboratory, The Fourth Affiliated Hospital to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215028, People’s Republic of China
Correspondence: Yafeng Zhou, Email Dryafengzhou@163.com Huimin Fan, Email fhm_sunshine@163.com
Abstract: Acute myocardial infarction (AMI) remains one of the leading causes of mortality and disability worldwide, involving complex immune and inflammatory responses. Among these, macrophages play a pivotal role as key immune cells. The polarization state of macrophages determines their function in both myocardial injury and repair. In the early phase of AMI, M1 macrophages promote inflammation and facilitate the clearance of necrotic tissue by releasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). However, excessive or prolonged M1 polarization may contribute to myocardial fibrosis and further deterioration of cardiac function. In contrast, M2 macrophages promote tissue repair and anti-inflammatory responses in the later phase by secreting anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β), thereby reducing fibrosis and facilitating myocardial remodeling. This review summarizes the dynamic changes in macrophage polarization during AMI and elaborates on their roles in myocardial injury, inflammation, and tissue repair. Furthermore, it highlights recent advances in therapeutic strategies aimed at modulating macrophage polarization to improve AMI outcomes, including mTOR inhibitors, sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and gene-editing technologies such as CRISPR/Cas9. Overall, this review underscores the importance of regulating macrophage polarization, particularly the transition from M1 to M2, as a promising therapeutic target for AMI. Modulating macrophage function may provide novel insights into enhancing myocardial repair and preventing adverse cardiac events.
Keywords: acute myocardial infarction, myocardial remodeling, macrophage polarization, M1/M2 macrophages, macrophage-based therapeutic strategies
1Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, 215000, People’s Republic of China; 2Department of Hypertension, The Fourth Affiliated Hospital of Soochow University, Institute for Hypertension, Soochow University, Suzhou, 215000, People’s Republic of China; 3Center of Translational Medicine and Clinical Laboratory, The Fourth Affiliated Hospital to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215028, People’s Republic of China
Correspondence: Yafeng Zhou, Email Dryafengzhou@163.com Huimin Fan, Email fhm_sunshine@163.com
Abstract: Acute myocardial infarction (AMI) remains one of the leading causes of mortality and disability worldwide, involving complex immune and inflammatory responses. Among these, macrophages play a pivotal role as key immune cells. The polarization state of macrophages determines their function in both myocardial injury and repair. In the early phase of AMI, M1 macrophages promote inflammation and facilitate the clearance of necrotic tissue by releasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). However, excessive or prolonged M1 polarization may contribute to myocardial fibrosis and further deterioration of cardiac function. In contrast, M2 macrophages promote tissue repair and anti-inflammatory responses in the later phase by secreting anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β), thereby reducing fibrosis and facilitating myocardial remodeling. This review summarizes the dynamic changes in macrophage polarization during AMI and elaborates on their roles in myocardial injury, inflammation, and tissue repair. Furthermore, it highlights recent advances in therapeutic strategies aimed at modulating macrophage polarization to improve AMI outcomes, including mTOR inhibitors, sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and gene-editing technologies such as CRISPR/Cas9. Overall, this review underscores the importance of regulating macrophage polarization, particularly the transition from M1 to M2, as a promising therapeutic target for AMI. Modulating macrophage function may provide novel insights into enhancing myocardial repair and preventing adverse cardiac events.
Keywords: acute myocardial infarction, myocardial remodeling, macrophage polarization, M1/M2 macrophages, macrophage-based therapeutic strategies