心力衰竭(heart failure, HF)是各种心血管疾病的终末阶段, 核心特征之一是心肌细胞的结构与功能紊乱。近年来,随着分子生物学与基因技术的发展, 研究视角已从宏观的器官功能衰竭深入至微观的基因表达调控、代谢重构、免疫炎症反应、细胞外基质与细胞骨架蛋白的动态变化等。细胞骨架蛋白作为心肌细胞的“内部支架”,其在HF发生发展中的关键作用日益凸显。本综述旨在系统梳理心肌细胞骨架(包括微丝、微管和中间丝)和细胞外基质在HF中的病理重塑、分子机制及作为潜在治疗靶点的研究现状,并展望未来研究方向,期望为HF的基础研究和临床治疗提供新的理论依据。

Heart failure (HF) represents the terminal stage of various cardiovascular diseases, and one of its core characteristics is the structural and functional disorders of cardiomyocytes. In recent years, with the advancement of molecular biology and genetic technologies, the research focus has shifted from the macroscopic organ failure to the microscopic molecular networks, including gene expression regulation, metabolic remodeling, immune-inflammatory responses, and dynamic changes in the extracellular matrix and cytoskeletal proteins. As the "internal scaffold" of cardiomyocytes, cytoskeletal proteins have increasingly demonstrated their critical role in the occurrence and progression of HF. This review aims to systematically summarize the current research status of pathological remodeling, molecular mechanisms, and potential therapeutic targets of the cardiomyocyte cytoskeleton (including microfilaments, microtubules, and intermediate filaments) as well as the extracellular matrix in HF. It also outlooks future research directions, providing references for the basic research and clinical treatment of HF, with the expectation of offering new theoretical foundations and directions for the precise prevention and treatment of HF.