Perrucci Gianluca Lorenzo, Rurali Erica, Pompilio Giulio
Dipartimento di Scienze Cliniche e di Comunità, Università degli Studi di Milano, Milano, Italy.
Unità di Biologia Vascolare e Medicina Rigenerativa, Centro Cardiologico Monzino-IRCCS, Milano, Italy.
J Thorac Dis. 2018 Jul;10(Suppl 20):S2376-S2389. doi: 10.21037/jtd.2018.03.82.
The major limitations for cardiac regeneration in patients after myocardial infarction (MI) are the wide loss of cardiomyocytes and the adverse structural alterations of extracellular matrix (ECM). Cardiac fibroblast differentiation into myofibroblasts (MFB) leads to a huge deposition of ECM and to the subsequent loss of ventricular structural integrity. All these molecular events depict the fundamental features at the basis of the post-MI fibrosis and deserve in depth cellular and molecular studies to fill the gap in the clinical practice. Indeed, to date, there are no effective therapeutic approaches to limit the post-MI massive fibrosis development. In this review we describe the involvement of integrins and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)/ADAMTS-like (ADAMTSL) proteins in cardiac reparative pro-fibrotic response after MI, proposing some of them as novel potential pharmacological tools.
心肌梗死（MI）后患者心脏再生的主要限制因素是心肌细胞的大量丧失以及细胞外基质（ECM）的不良结构改变。心脏成纤维细胞分化为肌成纤维细胞（MFB）会导致ECM大量沉积，并随后导致心室结构完整性丧失。所有这些分子事件描绘了MI后纤维化的基本特征，值得进行深入的细胞和分子研究以填补临床实践中的空白。事实上，迄今为止，尚无有效的治疗方法来限制MI后大量纤维化的发展。在本综述中，我们描述了整合素和含血小板反应蛋白基序的解聚素和金属蛋白酶（ADAMTS）/类ADAMTS（ADAMTSL）蛋白在MI后心脏修复性促纤维化反应中的作用，提出其中一些可作为新型潜在的药理学工具。
