Department of Medicine, Division of Cardiovascular Medicine, Institute of Molecular Cardiology, University of Louisville, 580 S. Preston St., Rm 122, Louisville, KY 40202, USA.
Department of Cardiovascular Medicine, Faculty of Medicine, Zagazig University, Zagazig 44519, Egypt.
Int J Mol Sci. 2021 Jul 19;22(14):7720. doi: 10.3390/ijms22147720.
Unlike some lower vertebrates which can completely regenerate their heart, the human heart is a terminally differentiated organ. Cardiomyocytes lost during cardiac injury and heart failure cannot be replaced due to their limited proliferative capacity. Therefore, cardiac injury generally leads to progressive failure. Here, we summarize the latest progress in research on methods to induce cardiomyocyte cell cycle entry and heart repair through the alteration of cardiomyocyte plasticity, which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart functions.
与一些能够完全再生心脏的低等脊椎动物不同，人类心脏是一个终末分化的器官。由于心肌细胞的增殖能力有限，在心脏损伤和心力衰竭时丢失的心肌细胞无法被替代。因此，心脏损伤通常会导致进行性衰竭。在这里，我们总结了通过改变心肌细胞的可塑性来诱导心肌细胞进入细胞周期和心脏修复的最新研究进展，这正在成为补偿功能性心肌细胞损失和改善受损心脏功能的有效策略。
