TBC1D15 and ischemic cardiomyopathy: Previous studies have found that loss of TBC1D15 resulted in abnormal mitochondria-lysosome contact sites observed in heart tissues from patients with ischemic cardiomyopathy (ICM), and from mouse hearts of ischemia/reperfusion (I/R) and neonatal mouse cardiomyocytes (NMCMs) exposed to hypoxia/reoxygenation (H/R), and this abnormality was improved by TBC1D15 overexpression.