Diastolic dysfunction, defined by increased ventricular stiffness, is a common pathological feature across diverse forms of heart disease and a major contributor to clinical syndromes such as heart failure with preserved ejection fraction. However, the cardiomyocyte-intrinsic mechanisms that lead to diastolic dysfunction remain incompletely understood. We found SORBS2 as a cardiomyocyte-intrinsic regulator of diastolic function. To reveal the underlying mechanism, we used proximity proteomics in intact, living hearts to identify proteins enriched near SORBS2.