CACNA1C and cardiac hypertrophy: In contrast, with specific overexpression of a caveolae-targeted CaV1.2 inhibitor (CBD-REM, a truncated REM1-265 fused N-terminal to caveolin-binding domain) or activator (CBD-β2a, a mutated β2aC3S/C4S fused C-terminal to CBD) in cardiac muscles, the transgenic mice subject to the transverse aortic constriction model did not show significant changes in hypertrophic signaling and cardiac function [35], suggesting that, at least in adult mouse heart, the caveolae-resident CaV1.2 channels may not contribute to the development of cardiac hypertrophy.