
上海交通大学学报(医学版) ›› 2026, Vol. 46 ›› Issue (3): 368-376.doi: 10.3969/j.issn.1674-8115.2026.03.011
• 综述 • 上一篇
赵旻炅1, 陈铃芳1, 胡苗清1, 冯杰1,2, 聂宇1,2(
)
收稿日期:2025-07-31
接受日期:2025-12-01
出版日期:2026-03-28
发布日期:2026-03-30
通讯作者:
聂 宇,研究员,博士;电子信箱:nieyuniverse@126.com。基金资助:
Zhao Minjiong1, Chen Lingfang1, Hu Miaoqing1, Feng Jie1,2, Nie Yu1,2(
)
Received:2025-07-31
Accepted:2025-12-01
Online:2026-03-28
Published:2026-03-30
Contact:
Nie Yu, E-mail: nieyuniverse@126.com.Supported by:摘要:
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。
中图分类号:
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.
Zhao Minjiong, Chen Lingfang, Hu Miaoqing, Feng Jie, Nie Yu. Research progress on immune cells regulation of cardiac regeneration after ischemic myocardial injury[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(3): 368-376.
图1 参与心肌损伤后修复与再生的免疫细胞及其效应分子Note: The outer ring sequentially illustrates neutrophils, monocytes (Ly6ChighCCR2+, Ly6Clow), macrophages (CCR2- reparative, CCR2+ pro-inflammatory), T cells (CD8+, Th1/Th17, Treg, Th2), and B cells. Neutrophils are rapidly recruited post-injury to clear necrotic debris and amplify acute inflammation via the S100A8/A9-TLR4-NLRP3-IL-1β axis, subsequently contributing to the resolution of inflammation. Early-stage Ly6ChighCCR2+ monocytes are primarily responsible for phagocytosis and clearance; subsequently, Ly6Clow monocytes and their differentiated reparative macrophages synergistically promote tissue reconstruction and angiogenesis. Resident CCR2- reparative macrophages directly drive cardiomyocyte dedifferentiation and proliferation via the OSM-OSMR/gp130-SRC-YAP (Y357) pathway, while also promoting homeostasis and angiogenesis through efferocytosis and IGF1/IGF2 secretion. Transiently appearing CCR2+ pro-inflammatory macrophages secrete IL-6, serving as a critical trigger signal for the regenerative response. In adaptive immunity, CD8+ T cells and Th1/Th17 subsets (associated with IFN-γ and IL-17) inhibit regeneration. Conversely, Tregs (secreting IL-10, TGF-β, AREG, and GAS6) and Th2 cells (secreting IL-4 and IL-13) support cardiomyocyte proliferation and functional recovery by remodelling the immune microenvironment and exerting direct or indirect regulatory effects. Neonatal B cells (including the S100A6highS100A4high subset) secrete various factors to promote cardiomyocyte proliferation.
Fig 1 Immune cells and their effector molecules involved in repair and regeneration after myocardial injury
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