收稿日期: 2025-07-31
录用日期: 2025-12-01
网络出版日期: 2026-03-30
基金资助
国家自然科学基金(82300325);国家心血管病中心华中分中心自主课题(2024-FZX04);心血管疾病全国重点实验室资助项目(2025GZZD-03);心血管疾病全国重点实验室资助项目(2025GZQN-04);中国医学科学院中央级公益性科研院所基本科研业务费(2023-PT310-03)
Research progress on immune cells regulation of cardiac regeneration after ischemic myocardial injury
Received date: 2025-07-31
Accepted date: 2025-12-01
Online published: 2026-03-30
Supported by
National Natural Science Foundation of China(82300325);The Grants from Henan Cardiovascular Disease Center (Central China Subcenter of National Center for Cardiovascular Diseases)(2024-FZX04);The State Key Laboratory of Cardiovascular Disease(2025GZZD-03);The Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences(2023-PT310-03)
缺血性心脏病特别是心肌梗死可导致大量心肌细胞不可逆性丧失。由于成年哺乳动物心肌细胞增殖能力高度受限，心肌受损区域通常被纤维化瘢痕组织取代，进而引发心室重构和心力衰竭，对健康造成严重威胁。近年来，诱导内源性心肌再生已成为改善心肌损伤预后的潜在治疗策略，而免疫调控机制在其中发挥核心作用。心肌损伤后，机体迅速启动复杂的炎症免疫级联反应。研究表明，炎症反应的时序与强度是决定组织修复结局的关键。在具有再生能力的模型中炎症反应启动迅速且消退及时，而成年个体则常出现炎症消退延迟与免疫失调，导致纤维化瘢痕形成。在此过程中，多种免疫细胞（如巨噬细胞、中性粒细胞、T细胞等）凭借其高度异质性特征、时序性浸润模式及微环境特异性分布，通过细胞间直接接触或旁分泌途径等方式，精细调控心肌细胞增殖与组织修复进程。这些免疫调控机制相互协调，形成一个动态促进心肌再生的交互网络。该综述系统阐述了各类免疫细胞在心肌损伤后再生修复过程中的应答特征及其调控机制，以期为缺血性心脏病的临床治疗提供新的思路与策略。
赵旻炅 , 陈铃芳 , 胡苗清 , 冯杰 , 聂宇 . 免疫细胞调控心肌缺血损伤后再生的研究进展[J]. 上海交通大学学报（医学版）, 2026 , 46(3) : 368 -376 . DOI: 10.3969/j.issn.1674-8115.2026.03.011
Ischemic heart disease, particularly myocardial infarction, can lead to extensive and irreversible loss of cardiomyocytes. Due to the highly restricted proliferative capacity of cardiomyocytes in adult mammals, the damaged myocardial regions are typically replaced by fibrotic scar tissue, leading to ventricular remodelling and heart failure, which poses a serious threat to health. In recent years, promoting endogenous cardiac regeneration has emerged as an attractive strategy to improve outcomes following myocardial injury, and immune regulatory mechanisms play a central role in this process. Upon myocardial injury, the body initiates a complex inflammatory immune cascade. Studies have shown that the timing and magnitude of the inflammatory responses are critical determinants of tissue repair outcomes. In regenerative models, inflammatory responses initiate rapidly and resolve promptly, whereas in adults, inflammation often persists, and immune dysregulation leads to fibrotic scar formation. During this process, various immune cells (such as macrophages, neutrophils, and T cells) exert precise regulation on cardiomyocyte proliferation and tissue repair through direct intercellular contact or paracrine signalling pathways. This is achieved via their highly heterogeneous characteristics, sequential infiltration patterns, and microenvironment-specific distribution. These immune regulatory mechanisms coordinate to form a dynamic and interactive network that promotes cardiac regeneration. This review systematically summarises the response characteristics and regulatory mechanisms of various immune cells during the regenerative repair process following myocardial injury, aiming to provide novel insights and strategies for the clinical treatment of ischemic heart disease.
Key words： immune cell; inflammatory response; immunoregulation; cardiac regeneration
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