Laboratory Animal Center and Department of Biochemistry, Institute of Guangdong Engineering and Technology Research Center for Disease-Model Animals, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China.
Cell Rep. 2022 Mar 8;38(10):110468. doi: 10.1016/j.celrep.2022.110468.
As a biological pump, the heart needs to consume a substantial amount of energy to maintain sustained beating. Myocardial energy metabolism was recently reported to be related to the loss of proliferative capacity in cardiomyocytes (CMs). However, the intrinsic relationship between beating rate and proliferation in CMs and whether energy metabolism can regulate this relationship remains unclear. In this study, we find that moderate heart rate reduction (HRR) induces CM proliferation under physiological conditions and promotes cardiac regenerative repair after myocardial injury. Mechanistically, moderate HRR induces G1/S transition and increases the expression of glycolytic enzymes in CMs. Furthermore, moderate HRR induces a metabolic pattern switch, activating glucose metabolism and increasing the relative proportion of ATP production by the glycolytic pathway for biosynthesis of substrates needed for proliferative CMs. These results highlight the potential therapeutic role of HRR in not only acute myocardial protection but also long-term CM restoration.
作为一个生物泵,心脏需要消耗大量的能量来维持持续的跳动。最近有研究报道,心肌能量代谢与心肌细胞(CMs)增殖能力的丧失有关。然而,CMs 的跳动率与增殖之间的内在关系,以及能量代谢是否可以调节这种关系尚不清楚。在这项研究中,我们发现适度的心率降低(HRR)在生理条件下诱导 CM 增殖,并促进心肌损伤后的心脏再生修复。在机制上,适度的 HRR 诱导 G1/S 期转换,并增加 CM 中糖酵解酶的表达。此外,适度的 HRR 诱导代谢模式转换,激活葡萄糖代谢,增加糖酵解途径产生合成增殖 CM 所需底物的 ATP 生成的相对比例。这些结果强调了 HRR 在急性心肌保护以及长期 CM 恢复中的潜在治疗作用。