5th Department of Internal Medicine, University Hospital Bratislava-Ružinov, Bratislava, Slovakia.
Physiol Res. 2021 Nov 30;70(Suppl 1):S13-S20.
Heart remodeling occurs as a compensation mechanism for the massive loss of tissue during initial heart failure and the consequent inflammation process. During heart remodeling fibroblasts differentiate to myofibroblasts activate their secretion functions and produce elevated amounts, of extracellular matrix (ECM) proteins, mostly collagen, that form scar tissue and alter the normal degradation of ECM. Scar formation does replace the damaged tissue structurally; however, it impedes the normal contractive function of cardiomyocytes (CMs) and results in long-lasting effects after heart failure. Besides CMs and cardiac fibroblasts, endothelial cells (ECs) and circulating endothelial progenitor cells (cEPCs) contribute to heart repair. This review summarizes the current knowledge of EC-CM crosstalk in cardiac fibrosis (CF), the role of cEPCs in heart regeneration and the contribution of Endothelial-mesenchymal transition (EndoMT).
心脏重构是心肌初始衰竭和随之发生的炎症过程中大量组织丢失的代偿机制。在心脏重构过程中，成纤维细胞分化为肌成纤维细胞，激活其分泌功能，并产生大量细胞外基质 (ECM) 蛋白，主要是胶原蛋白，形成瘢痕组织，并改变 ECM 的正常降解。瘢痕形成确实在结构上替代了受损组织；然而，它阻碍了心肌细胞 (CMs) 的正常收缩功能，并在心衰后产生持久的影响。除了 CMs 和心脏成纤维细胞外，内皮细胞 (ECs) 和循环内皮祖细胞 (cEPCs) 也有助于心脏修复。本文综述了 ECM 与心脏纤维化 (CF) 中内皮细胞的相互作用、cEPCs 在心脏再生中的作用以及内皮-间充质转化 (EndoMT) 的贡献。
