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.

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。