| Автор | Dong, Zheng |
| Автор | Saikumar, Pothana |
| Автор | Weinberg, Joel M. |
| Автор | Venkatachalam, Manjeri A. |
| Дата выпуска | 2006 |
| dc.description | Abstract Loss of Ca<sup>2+</sup> homeostasis, often in the form of cytoplasmic increases, leads to cell injury. Depending upon cell type and the intensity of Ca<sup>2+</sup> toxicity, the ensuing pathology can be reversible or irreversible. Although multiple destructive processes are activated by Ca<sup>2+</sup>, lethal outcomes are determined largely by Ca<sup>2+</sup>-induced mitochondrial permeability transition. This form of damage is primarily dependent upon mitochondrial Ca<sup>2+</sup> accumulation, which is regulated by the mitochondrial membrane potential. Retention of the mitochondrial membrane potential during Ca<sup>2+</sup> increases favors mitochondrial Ca<sup>2+</sup> uptake and overload, resulting in mitochondrial permeability transition and cell death. In contrast, dissipation of mitochondrial membrane potential reduces mitochondrial Ca<sup>2+</sup> uptake, retards mitochondrial permeability transition, and delays death, even in cells with large Ca<sup>2+</sup> increases. The rates of mitochondrial membrane potential dissipation and mitochondrial Ca<sup>2+</sup> uptake may determine cellular sensitivity to Ca<sup>2+</sup> toxicity under pathological conditions, including ischemic injury. |
| Формат | application.pdf |
| Издатель | Annual Reviews |
| Копирайт | Annual Reviews |
| Название | CALCIUM IN CELL INJURY AND DEATH * |
| DOI | 10.1146/annurev.pathol.1.110304.100218 |
| Print ISSN | 1553-4006 |
| Журнал | Annual Review of Pathology: Mechanisms of Disease |
| Том | 1 |
| Первая страница | 405 |
| Последняя страница | 434 |
| Аффилиация | Dong, Zheng; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912; Medical Research Service, Department of Veterans Affairs Medical Center, Augusta, Georgia 30904; email: zdong@mcg.edu |
