Endothelial-Mesenchymal Transition or Functional Tissue Regeneration – Two Outcomes of Heart Remodeling

Abstract

Heart remodeling occurs as a compensation mechanism for themassive loss of tissue during initial heart failure and theconsequent inflammation process. During heart remodelingfibroblasts differentiate to myofibroblasts activate their secretionfunctions and produce elevated amounts, of extracel lular matrix(ECM) proteins, mostly collagen, that form scar tissue and alterthe normal degradation of ECM. Scar formation does replace thedamaged tissue structurally; however, it impedes the normalcontractive function of cardiomyocytes (CMs) and results in longlastingeffects after heart failure. Besides CMs and cardiacfibroblasts, endothelial cells (ECs) and circulating endothelialprogenitor cells (cEPCs) contribute to heart repair. This reviewsummarizes the current knowledge of EC-CM crosstalk in cardiacfibrosis (CF), the role of cEPCs in heart regeneration and thecontribution of Endothelial-mesenchymal transition (EndoMT)