fig6

Figure 6. Lysosome-mitochondria communication in cardiomyocytes under physiological and aging conditions. In healthy cardiomyocytes, transient contact sites between mitochondria and lysosomes are regulated by Rab7 in its GTP-bound active state and its effector TBC1D15, which is recruited to the mitochondrial surface via the fission protein Fis1. These contacts contribute to mitochondrial dynamics, mitophagy, and cellular homeostasis. Conversely, in aged or stressed cardiomyocytes, impaired recruitment of TBC1D15 or dysregulation of Rab7 activity leads to prolonged or unstable contacts, defective mitophagy, and altered mitochondrial fission, resulting in the accumulation of dysfunctional mitochondria and elevated oxidative stress. These alterations contribute to mitochondrial dysfunction, impaired cardiomyocyte contractility, and the progression of age-related cardiovascular diseases.