Esketamine alleviates hypoxia/reoxygenation injury of cardiomyocytes by regulating TRPV1 expression and inhibiting intracellular Ca2+ concentration

Zhang, Ying; Lu, QuanMei; Hu, HanChun; Yang, ChunChen; Zhao, QiHong

doi:10.1016/j.clinsp.2024.100363

Cited by 1 publication

(1 citation statement)

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“…After myocardial ischemia/reperfusion injury (I/R), a study found that cardiomyocyte viability decreased, cell apoptosis increased, and intracellular Ca 2+ concentration rose. The upregulation of TRPV1 decreases cardiomyocyte viability and increases apoptosis and intracellular Ca 2+ concentration, while the downregulation of TRPV1 further prevents I/R damage [ 51 ]. Other studies have shown that downregulated TRPV2 can significantly inhibit ROS production and Ca 2+ concentration in cardiomyocytes.…”

Section: Ion Channel Changes After MImentioning

confidence: 99%

Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges

Song,

Hui,

Huang

et al. 2024

IJMS

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In different areas of the heart, action potential waveforms differ due to differences in the expressions of sodium, calcium, and potassium channels. One of the characteristics of myocardial infarction (MI) is an imbalance in oxygen supply and demand, leading to ion imbalance. After MI, the regulation and expression levels of K+, Ca2+, and Na+ ion channels in cardiomyocytes are altered, which affects the regularity of cardiac rhythm and leads to myocardial injury. Myocardial fibroblasts are the main effector cells in the process of MI repair. The ion channels of myocardial fibroblasts play an important role in the process of MI. At the same time, a large number of ion channels are expressed in immune cells, which play an important role by regulating the in- and outflow of ions to complete intracellular signal transduction. Ion channels are widely distributed in a variety of cells and are attractive targets for drug development. This article reviews the changes in different ion channels after MI and the therapeutic drugs for these channels. We analyze the complex molecular mechanisms behind myocardial ion channel regulation and the challenges in ion channel drug therapy.

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Section: Ion Channel Changes After MImentioning

confidence: 99%