ArticleHerz2026
Tetrandrine has protective role in myocardial ischemia/reperfusion injury via the TRPV2/Ca
Article in Herz, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
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Abstract
backgroundThe protective function of the tetrandrine (TET)-mediated transient receptor potential vanilloid 2 (TRPV2) channel in myocardial ischemia/reperfusion injury (MI/RI) has been established in numerous investigations. The objective of the current study was to explain how TRPV2 further modulates downstream factors to influence the progression of MI/RI.
methodsTo this end, an MI/RI model in rats and a hypoxia-reoxygenation (H/R) cell model in H9c2 cells were constructed. Based on western blotting analyses, the effects of TRPV2 on the levels of apoptosis-related proteins as well as calcineurin and nuclear factor of activated T cells (NFAT) were ascertained. Evans blue/triphenyltetrazolium chloride (TTC) double staining and H&E staining were, respectively, used to examine the pathological changes and infarction size of myocardial tissues in rats. Cardiomyocyte apoptosis was assessed with TUNEL assays and flow cytometry. Ca
resultsDownregulated TRPV2 showed a significant ameliorative effect on cardiomyocyte histopathology and infarction area. Cardiomyocyte apoptosis, Ca
conclusionThese findings shed light on the possible mechanisms behind the TET-mediated TRPV2 channel in MI/RI, indicating that TET has protective functions through downregulation of TRPV2 expression and suppression of the Ca
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