Burdock Group, 859 Outer Road, Orlando, FL 32814, USA.
Department of Physiology, Brody School of Medicine, 600 Moye Blvd, East Carolina University, Greenville, NC 27834, USA.
Int J Mol Sci. 2019 Mar 22;20(6):1449. doi: 10.3390/ijms20061449.
Myocardial tissue damage that occurs during an ischemic event leads to a spiraling deterioration of cardiac muscle structural and functional integrity. Reperfusion is the only known efficacious strategy and is the most commonly used treatment to reduce injury and prevent remodeling. However, timing is critical, and the procedure is not always feasible for a variety of reasons. The complex molecular basis for cardioprotection has been studied for decades but formulation of a viable therapeutic that can significantly attenuate myocardial injury remains elusive. In this review, we address barriers to the development of a fruitful approach that will substantially improve the prognosis of those suffering from this widespread and largely unmitigated disease. Furthermore, we proffer that ephrinA1, a candidate molecule that satisfies many of the important criteria discussed, possesses robust potential to overcome these hurdles and thus offers protection that surpasses the limitations currently observed.
缺血事件发生时心肌组织损伤会导致心肌结构和功能完整性的螺旋式恶化。再灌注是唯一已知有效的策略，也是减少损伤和预防重构的最常用治疗方法。然而，时机至关重要，由于各种原因，该程序并非总是可行。几十年来，人们一直在研究心脏保护的复杂分子基础，但制定一种可行的治疗方法来显著减轻心肌损伤仍然难以捉摸。在这篇综述中，我们讨论了开发一种有成效的方法的障碍，该方法将大大改善那些患有这种广泛且在很大程度上未得到缓解的疾病的人的预后。此外，我们提出，ephrinA1 是一种候选分子，它满足了许多讨论过的重要标准，具有克服这些障碍的强大潜力，从而提供了超越目前观察到的限制的保护。
