Xia Huiting, Zahra Aqeela, Jia Meng, Wang Qun, Wang Yunfu, Campbell Susan L, Wu Jianping
School of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan 430070, China.
Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China.
Pharmaceuticals (Basel). 2022 Jul 15;15(7):875. doi: 10.3390/ph15070875.
Cardiac hypertrophy is defined as increased heart mass in response to increased hemodynamic requirements. Long-term cardiac hypertrophy, if not counteracted, will ultimately lead to heart failure. The incidence of heart failure is related to myocardial infarction, which could be salvaged by reperfusion and ultimately invites unfavorable myocardial ischemia-reperfusion injury. The Na/H exchangers (NHEs) are membrane transporters that exchange one intracellular proton for one extracellular Na. The first discovered NHE isoform, NHE1, is expressed almost ubiquitously in all tissues, especially in the myocardium. During myocardial ischemia-reperfusion, NHE1 catalyzes increased uptake of intracellular Na, which in turn leads to Ca overload and subsequently myocardial injury. Numerous preclinical research has shown that NHE1 is involved in cardiac hypertrophy and heart failure, but the exact molecular mechanisms remain elusive. The objective of this review is to demonstrate the potential role of NHE1 in cardiac hypertrophy and heart failure and investigate the underlying mechanisms.
心脏肥大被定义为心脏质量增加以应对血流动力学需求增加。长期的心脏肥大如果不加以对抗，最终将导致心力衰竭。心力衰竭的发生率与心肌梗死有关，心肌梗死可通过再灌注挽救，但最终会引发不利的心肌缺血-再灌注损伤。钠/氢交换体（NHEs）是一种膜转运蛋白，可将一个细胞内质子与一个细胞外钠离子进行交换。最早发现的NHE亚型NHE1几乎在所有组织中广泛表达，尤其是在心肌中。在心肌缺血-再灌注期间，NHE1催化细胞内钠离子摄取增加，进而导致钙超载并随后引发心肌损伤。大量临床前研究表明，NHE1参与心脏肥大和心力衰竭，但确切的分子机制仍不清楚。本综述的目的是阐述NHE1在心脏肥大和心力衰竭中的潜在作用，并研究其潜在机制。
