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Annu Rev Pathol. 2006;1:405-34.

Calcium in cell injury and death.

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1
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912, USA. zdong@mcg.edu

Abstract

Loss of Ca(2+) homeostasis, often in the form of cytoplasmic increases, leads to cell injury. Depending upon cell type and the intensity of Ca(2+) toxicity, the ensuing pathology can be reversible or irreversible. Although multiple destructive processes are activated by Ca(2+), lethal outcomes are determined largely by Ca(2+)-induced mitochondrial permeability transition. This form of damage is primarily dependent upon mitochondrial Ca(2+) accumulation, which is regulated by the mitochondrial membrane potential. Retention of the mitochondrial membrane potential during Ca(2+) increases favors mitochondrial Ca(2+) uptake and overload, resulting in mitochondrial permeability transition and cell death. In contrast, dissipation of mitochondrial membrane potential reduces mitochondrial Ca(2+) uptake, retards mitochondrial permeability transition, and delays death, even in cells with large Ca(2+) increases. The rates of mitochondrial membrane potential dissipation and mitochondrial Ca(2+) uptake may determine cellular sensitivity to Ca(2+) toxicity under pathological conditions, including ischemic injury.

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