癌症进展的一个重要机制是细胞外基质（ECM）的降解，伴随着活化的成纤维细胞（称为癌症相关成纤维细胞（CAF））的出现和增殖。更具体地说，成纤维细胞激活蛋白（FAP）被认为是随着局部癌症进展和 CAF 增殖而放大的酶途径。无论病因如何，心力衰竭 (HF) 的发生和进展都与左心室 (LV) 重塑以及 ECM 结构和功能的变化相关。与癌症一样，心力衰竭的进展与左心室心肌成纤维细胞生长和功能的变化相关，并表达与 CAF 相似的蛋白质特征。本综述的总体目标是提出这样一个假设：关于癌症中 FAP 的科学发现以及特定化疗药物的开发可以针对活化成纤维细胞亚型中 FAP 的出现，从而掌握转化相关的诊断和治疗靶点HF 中。版权所有 © 2023。由 Elsevier Inc. 出版。

An important mechanism for cancer progression is degradation of the extracellular matrix (ECM) which is accompanied by the emergence and proliferation of an activated fibroblast, termed the cancer associated fibroblast (CAF). More specifically, an enzyme pathway identified to be amplified with local cancer progression and proliferation of the CAF, is fibroblast activation protein (FAP). The development and progression of heart failure (HF) irrespective of the etiology is associated with left ventricular (LV) remodeling and changes in ECM structure and function. As with cancer, HF progression is associated with a change in LV myocardial fibroblast growth and function, and expresses a protein signature not dissimilar to the CAF. The overall goal of this review is to put forward the postulate that scientific discoveries regarding FAP in cancer as well as the development of specific chemotherapeutics could be pivoted to target the emergence of FAP in the activated fibroblast subtype and thus hold translationally relevant diagnostic and therapeutic targets in HF.Copyright © 2023. Published by Elsevier Inc.