A background Ca²⁺entry pathway mediated by TRPC1/TRPC4 is critical for development of pathological cardiac remodelling

Abstract

The constitutively active TRPC1/C4-dependent BGCE fine-tunes Ca(2+) cycling in beating adult cardiomyocytes. TRPC1/C4-gene inactivation protects against development of maladaptive cardiac remodelling without altering cardiac or extracardiac functions contributing to this pathogenesis.