Overexpression of MIC60 in rat cardiomyocytes under extracellular acidosis (pH 6.5) preserves mitochondrial membrane potential, increases ATP production, improves cell viability, and reduces structural damage to mitochondrial cristae.

When the environment around heart cells becomes too acidic, a key protein called MIC60 starts breaking down, which damages the internal structure of mitochondria. This damage stops mitochondria from making energy properly and causes cells to die. A protective protein binds to MIC60 and stops it from being destroyed, allowing it to keep the mitochondria's internal folds intact. With those folds preserved, mitochondria can maintain their electrical charge and keep producing energy, which keeps the heart cells alive and functioning.