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Regulation of the Na(+)/H(+) exchanger in the healthy and diseased myocardium.

机译:在健康和患病心肌中Na(+)/ H(+)交换子的调节。

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摘要

BACKGROUND: Na(+)/H(+) exchangers (NHE's) are membrane proteins that regulate ion fluxes, they extrude one intracellular proton in exchange for one extracellular sodium thereby regulating intracellular pH. Mammalian NHE's have nine isoforms, NHE1-NHE9. NHE1 is present in all mammalian cell and is the only isoform present in cardiomyocytes. NHE1 contributes to damage to the myocardium with ischemia and reperfusion and to heart hypertrophy. OBJECTIVE: To summarize the current state of knowledge with regard to regulation of NHE1 in the myocardium. METHODS: A review of relevant literature. RESULTS: Inhibition of NHE reduces ischemia-reperfusion damage and development of hypertrophy. Extracellular-signal-regulated kinase (ERK)-dependent phosphorylation activates NHE1 in the myocardium. Ischemia and subsequent reperfusion activates the ERK-dependent pathway and may lead to aggravation of damage. CONCLUSIONS: Elucidation of the regulatory pathway of NHE1 in the myocardium could lead to novel approaches to reduce heart hypertrophy and ischemia-reperfusion damage.
机译:背景:Na(+)/ H(+)交换剂(NHE's)是调节离子通量的膜蛋白,它们挤出一个细胞内质子来交换一种细胞外钠,从而调节细胞内pH。哺乳动物NHE具有9个亚型,即NHE1-NHE9。 NHE1存在于所有哺乳动物细胞中,并且是心肌细胞中存在的唯一同工型。 NHE1有助于缺血和再灌注对心肌的损害以及心脏肥大。目的:总结关于NHE1在心肌中调节的知识的现状。方法:相关文献综述。结果:抑制NHE可减少缺血再灌注损伤和肥大的发展。细胞外信号调节激酶(ERK)依赖性磷酸化激活心肌中的NHE1。缺血和随后的再灌注激活了ERK依赖性途径,并可能导致损害加重。结论:阐明心肌中NHE1的调节途径可能导致减少心脏肥大和缺血再灌注损伤的新方法。

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