5th Department of Internal Medicine, University Hospital Bratislava-Ružinov, Bratislava, Slovakia.
Physiol Res. 2021 Nov 30;70(Suppl 1):S13-S20. doi: 10.33549/physiolres.934780.
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时大量组织丢失和随后的炎症过程的一种代偿机制。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，产生大量细胞外基质 (ECM) 蛋白，主要是胶原蛋白，形成疤痕组织，并改变 ECM 的正常降解。疤痕组织的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，并导致心力衰竭后的长期影响。除了心肌细胞和成纤维细胞外，内皮细胞 (ECs) 和循环内皮祖细胞 (cEPCs) 也有助于心脏修复。本文综述了心脏纤维化 (CF) 中 EC-CM 相互作用的最新知识、cEPCs 在心脏再生中的作用以及内皮-间充质转化 (EndoMT) 的贡献。
