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Ca2+ is a critical second messenger that is required for several cellular processes. Cytosolic Ca2+ (cCa2+)transients are shaped by the mitochondria due to the highly negative membrane potential and through themitochondrial calcium uniporter (MCU). Mitochondrial Ca2+ (mCa2+) is utilized by the matrix dehydrogenases formaintaining cellular bioenergetics. Reciprocally, dysregulated elevation of cCa2+ under conditions of stroke,ischemia/reperfusion injury drives mCa2+ overload that in turn leads to mitochondrial permeability transition poreopening that triggers necrotic cell death.

UT Health San Antonio
Muniswamy, Madesh