Activation of endothelial TRPV4 worsens myocardial injury via apoptosis in ischemia-reperfusion, suggesting a therapeutic strategy.
Activation of endothelial TRPV4 CECs exacerbates post-IR vascular hyperpermeability and myocardial injury by impairing barrier integrity and promoting apoptosis. Targeting endothelial TRPV4 may represent a promising therapeutic strategy to mitigate myocardial IR injury.
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Zhang et al. (2025) studied this question.
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