In Mice Subjected to Chronic Stress, Exogenous cBIN1 Preserves Calcium-Handling Machinery and Cardiac Function.

•T-tubule cBIN1-microdomains are disrupted in hearts with concentric hypertrophy.•cBIN1 replacement therapy rescues t-tubule microdomains and reduces concentric hypertrophy in post-ISO hearts inducing a hyper-efficient phenotype similar to athletic hearts.•cBIN1-microdomains organize t-tubule Cav1.2 and SERCA2a distribution for improved contractility and lusitropy.•Exogenous cBIN1 is also effective in protecting cardiac contractility and lusitropy in mouse hearts subjected to pressure overload.