Activation of <scp>TRPV1</scp> attenuates high salt‐induced cardiac hypertrophy through improvement of mitochondrial function

Abstract

TRPV1 activation by dietary capsaicin can antagonize high-salt diet-mediated cardiac lesions by ameliorating its deleterious effect on the proficiency of Complex I OXPHOS. TRPV1-mediated amendment of mitochondrial dysfunction may represent a novel target for management of early cardiac dysfunction.