Background


The overarching aim of CalTIC is to generate novel lead compounds targeting TRPC´s with in vivo proof-of-concept (PoC) and lead optimisation potential.

Tetrameric Ca2+-permeable cation channels formed by TRPC proteins are genetically validated targets for pressure overload-induced hypertrophy and interstitial fibrosis in cardiac hypertrophy, a key feature of pathological cardiac remodeling associated with the development of cardiac failure. A background Ca2+-entry (BGCE) pathway that critically depends on representatives of the TRPC proteins family has been described. The constitutively active TRPC-dependent BGCE fine-tunes Ca2+ cycling in beating adult cardiomyocytes. TRPC-gene inactivation protects against development of maladaptive cardiac remodeling without altering cardiac or extracardiac functions contributing to this pathogenesis. Our research gives evidence to an additional role in obesity.