中国全科医学 ›› 2026, Vol. 29 ›› Issue (15): 2084-2091.DOI: 10.12114/j.issn.1007-9572.2024.0627

• 综述与专论 • 上一篇    

心脏巨噬细胞在射血分数保留型心力衰竭中的研究进展

李世龙1,2, 王贺1,2,*(), 周晓宇1,2, 付蕾1,2, 赵倬1,2, 华成俊1,2, 司春婴1,2   

  1. 1.450000 河南省郑州市,河南中医药大学第一附属医院心脏中心 国家区域(中医)心血管诊疗中心
    2.450000 河南省郑州市,河南中医药大学第一附属医院 中西医防治重大疾病河南省协同创新中心
  • 收稿日期:2024-09-10 修回日期:2025-01-10 出版日期:2026-05-20 发布日期:2026-04-14
  • 通讯作者: 王贺

  • 作者贡献:

    李世龙负责文章的构思与设计、研究资料的收集与整理、论文撰写;王贺和司春婴负责论文修订、文章的质量控制及审校、对文章整体负责;周晓宇和付蕾负责研究资料的收集与整理;赵倬和华成俊负责论文审阅及修订。

  • 基金资助:
    国家自然科学基金资助项目(82274316); 河南省自然科学基金资助项目(232300420273)

Advances in the Study of Cardiac Macrophages in Heart Failure with Preserved Ejection Fraction

LI Shilong1,2, WANG He1,2,*(), ZHOU Xiaoyu1,2, FU Lei1,2, ZHAO Zhuo1,2, HUA Chengjun1,2, SI Chunying1,2   

  1. 1. Heart Center, the First Affiliated Hospital of Henan University of CM/National Regional (Traditional Chinese Medicine) Cardiovascular Diagnosis and Treatment Center, Zhengzhou 450000, China
    2. The First Affiliated Hospital of Henan University of CM/Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine, Zhengzhou 450000, China
  • Received:2024-09-10 Revised:2025-01-10 Published:2026-05-20 Online:2026-04-14
  • Contact: WANG He

摘要: 射血分数保留型心力衰竭(HFpEF)是一种普遍且高度致命的全球性疾病,在心力衰竭患者中所占比例接近50%,需要创新方法来保护心脏功能并防止HFpEF进展。心脏巨噬细胞(CMs)已成为HFpEF病理生理学的关键调节因子。CMs是一个异质性群体,由具有不同谱系起源和基因表达谱的亚群组成。HFpEF进展的几个关键方面已被证明受CMs调节,包括外周免疫细胞的募集、心肌炎症以及心脏电传导。此外,CMs在调节心脏纤维化、心外膜脂肪组织功能障碍以及心室舒张功能障碍方面起着至关重要的作用。鉴于CMs在HFpEF病理生理学中的多方面作用,靶向调控CMs代表了一种很有前途的治疗策略。因此,本文将从心脏炎症和纤维化、心室舒张功能障碍、心外膜脂肪组织、心脏电传导以及临床干预几个方面对CMs与HFpEF病理生理机制的研究进展进行综述。

关键词: 射血分数保留型心力衰竭, 心力衰竭, 心脏巨噬细胞, 心外膜脂肪组织

Abstract:

Heart failure with preserved ejection fraction (HFpEF) is a universal and highly fatal global disease, accounting for nearly 50% of patients with heart failure. Innovative methods are needed to protect cardiac function and prevent the progression of HFpEF. Cardiac macrophages (CMs) have emerged as key regulators of the pathophysiology of HFpEF. CMs are a heterogeneous population consisting of subpopulations with distinct lineage origins and gene expression profiles. Several key aspects of HFpEF progression have been shown to be regulated by CMs, including the recruitment of peripheral immune cells, myocardial inflammation, and cardiac electrical conduction. In addition, CMs play a critical role in regulating cardiac fibrosis, epicardial adipose tissue dysfunction, and ventricular diastolic dysfunction. Given the multifaceted roles of CMs in the pathophysiology of HFpEF, targeted regulation of CMs represents a promising therapeutic strategy. Therefore, this article will review the research progress between CMs and the pathophysiological mechanism of HFpEF from the aspects of cardiac inflammation and fibrosis, ventricular diastolic dysfunction, epicardial adipose tissue, cardiac electrical conduction, and clinical intervention.

Key words: Heart failure with preserved ejection fraction, Heart failure, Cardiac macrophages, Epicardial adipose tissues

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