心肌梗死后心脏修复与心肌细胞再生的研究进展

心肌梗死后组织缺血缺氧,坏死,导致一个多相的修复过程,受损的组织由成纤维细胞和肌成纤维细胞产生纤维瘢痕所取代。非梗死的心室壁反应性重塑,包括间质和血管周围纤维化,导致心室壁几何、生物力学、生化等发生改变。虽然最初的修复性纤维化对防止心室壁破裂至关重要,但是过度的纤维化反应导致心功能进行性损害,最终导致心功能衰竭。近年来研究表明,心脏具有可塑性,恢复受损心脏功能,促进梗死心肌修复是心血管疾病治疗的重要目标。为此,人们不断探索新的治疗手段,再生治疗给心肌梗死治疗带来了新的希望,本文对目前心肌梗死的修复性及反应心肌纤维化的机制进行总结,探讨诱导成纤维细胞和肌成纤维细胞转化为心肌细胞,以及心肌细胞再生的潜力,对目前现有和未来抑制心肌纤维化治疗策略进行综述。

Recent advances in cardiac repair and regeneration after myocardial infarction

Myocardial ischemia, hypoxia and necrosis after myocardial infarction lead to a multiphase repair process in which damaged tissue is replaced with fibrous scars produced by fibroblasts and myofibroblasts. Non-infarct ventricular wall reactive remodeling, including interstitial and perivascular fibrosis, leads to changes in ventricular wall geometry, biomechanics, biochemistry and so on. Although initial repair fibrosis is essential to prevent ventricular wall rupture, excessive fibrosis leads to progressive damage to heart function and eventually to heart failure. Recent studies have shown that the heart has plasticity, restoring impaired cardiac function, and promoting myocardial repair after infarction are important targets for the treatment of cardiovascular diseases. To this end, people continue to explore new therapies, regeneration therapy for myocardial infarction treatment has brought new hope. This review summarizes the current myocardial infarction repair and reaction mechanism of cardiacl fibrosis, to explore the potential of inducing fibroblasts and myofibroblasts into cardiomtocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis.