Despite therapeutic advances that have prolonged life, myocardial infarction (MI) remains a leading cause of death worldwide and imparts a significant economic burden. The advancement of treatments to improve cardiac repair post-MI requires the discovery of new targeted treatment strategies. Recent studies have highlighted the importance of the epicardial covering of the heart in both cardiac development and lower vertebrate cardiac regeneration. The epicardium serves as a source of cardiac cells including smooth muscle cells, endothelial cells and cardiac fibroblasts. Mammalian adult epicardial cells are typically quiescent. However, the fetal genetic program is reactivated post-MI, and epicardial epithelial-to-mesenchymal transition (EMT) occurs as an inherent mechanism to support neovascularization and cardiac healing. Unfortunately, endogenous EMT is not enough to encourage sufficient repair. Recent developments in our understanding of the mechanisms supporting the EMT process has led to a number of studies directed at augmenting epicardial EMT post-MI. With a focus on the role of the primary cilium, this review outlines the newly demonstrated mechanisms supporting EMT, the role of epicardial EMT in cardiac development, and promising advances in augmenting epicardial EMT as potential therapeutics to support cardiac repair post-MI.

尽管可以延长寿命的治疗方法有所进步，但心肌梗塞（MI）仍然是全球范围内的主要死亡原因，并带来了巨大的经济负担。为了改善心梗后心脏修复的治疗进展需要发现新的靶向治疗策略。最近的研究突出了心脏的心外膜覆盖物在心脏发育和较低的脊椎动物心脏再生中的重要性。心外膜充当心脏细胞的来源，包括平滑肌细胞，内皮细胞和心脏成纤维细胞。哺乳动物成年心外膜细胞通常是静止的。但是，胎儿遗传程序在心梗后会重新激活，而心外膜上皮向间充质转变（EMT）作为支持新血管形成和心脏愈合的内在机制而发生。很遗憾，内源性EMT不足以鼓励充分修复。我们对支持EMT过程的机制的了解的最新进展导致了许多针对增加心梗后心外膜EMT的研究。着重于初级纤毛的作用，本综述概述了新近证明的支持EMT的机制，心外膜EMT在心脏发育中的作用，以及在增强心外膜EMT作为支持MI后心脏修复的潜在疗法方面的有希望的进展。