Why the study?
Cardiomyocyte Ca2+ homoeostasis is altered with ageing and predisposes the heart to arrhythmia, but the role of the osmotically activated cation channel TRPV4 in Ca2+ handling and arrhythmogenesis following ischaemia-reperfusion was unexamined.
TRPV4 inhibition reduces pro-arrhythmic Ca2+ signaling and ventricular arrhythmias following ischemia-reperfusion in aged mouse hearts.
TRPV4 inhibition merits further preclinical testing in aged I/R models; leaves open any role in human post-MI arrhythmia prevention.
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Peana et al. (2021) studied this question.
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