Calcium in cell injury and death

被引:216
作者
Dong, Zheng [1 ]
Saikumar, Pothana
Weinberg, Joel M.
Venkatachalam, Manjeri A.
机构
[1] Med Coll Georgia, Dept Anat & Cell Biol, Augusta, GA 30912 USA
[2] Dept Vet Affairs Med Ctr, Med Res Serv, Augusta, GA 30904 USA
[3] Univ Texas, Hlth Sci Ctr, Dept Pathol, San Antonio, TX 78229 USA
[4] Univ Michigan, Med Ctr, Dept Med, Ann Arbor, MI 48109 USA
[5] VA Ann Arbor VA Healthcare Syst, Ann Arbor, MI 48109 USA
关键词
mitochondria permeability transition; ischemia-reperfusion; apoptosis; adenosine triphosphate; glycine; nonesterified fatty acids;
D O I
10.1146/annurev.pathol.1.110304.100218
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Loss of Ca2+ homeostasis, often in the form of cytoplasmic increases, leads to cell injury. Depending upon cell type and the intensity of Ca2+ toxicity, the ensuing pathology can be reversible or irreversible. Although multiple destructive processes are activated by Ca2+, lethal outcomes are determined largely by Ca2+-induced mitochondria) permeability transition. This form of damage is primarily dependent upon mitochondrial Ca2+ accumulation, which is regulated by the mitochondria) membrane potential. Retention of the mitochondrial membrane potential during Ca2+ increases favors mitochondria) Ca2+ uptake and overload, resulting in mitochondrial permeability transition and cell death. In contrast, dissipation of mitochondrial membrane potential reduces mitochondrial Ca2+ uptake, retards mitochondrial permeability transition, and delays death, even in cells with large Ca2+ increases. The rates of mitochondrial membrane potential dissipation and mitochondrial Ca2+ uptake may determine cellular sensitivity to Ca2+ toxicity under pathological conditions, including ischemic injury
引用
收藏
页码:405 / 434
页数:30
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