Caveolin 3‐dependent loss of t‐tubular ICa during hypertrophy and heart failure in mice

New Findings What is the central question of this study? Heart failure is associated with redistribution of L‐type Ca2+ current (I Ca) away from the t‐tubule membrane to the surface membrane of cardiac ventricular myocytes. However, the underlying mechanism and its dependence on severity of pathology (hypertrophy versus failure) are unclear. What is the main finding and its importance? Increasing severity of response to transverse aortic constriction, from hypertrophy to failure, was accompanied by graded loss of t‐tubular I Ca and loss of regulation of I Ca by caveolin 3. Thus, the pathological loss of t‐tubular I Ca, which contributes to impaired excitation–contraction coupling and thereby cardiac function in vivo, appears to be attributable to loss of caveolin 3‐dependent stimulation of t‐tubular I Ca.