Calcium in cell injury and death

Zheng Dong, Pothana Saikumar, Joel M. Weinberg, Manjeri A. Venkatachalam

Research output: Contribution to journalReview article

167 Scopus citations

Abstract

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 Ca 2+, lethal outcomes are determined largely by Ca2+-induced mitochondrial permeability transition. This form of damage is primarily dependent upon mitochondrial Ca2+ accumulation, which is regulated by the mitochondrial membrane potential. Retention of the mitochondrial membrane potential during Ca2+ increases favors mitochondrial 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.

Original languageEnglish (US)
Pages (from-to)405-434
Number of pages30
JournalAnnual Review of Pathology
Volume1
DOIs
StatePublished - Apr 19 2006

Keywords

  • Adenosine triphosphate
  • Apoptosis
  • Glycine
  • Ischemia-reperfusion
  • Mitochondrial permeability transition
  • Nonesterified fatty acids

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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    Dong, Z., Saikumar, P., Weinberg, J. M., & Venkatachalam, M. A. (2006). Calcium in cell injury and death. Annual Review of Pathology, 1, 405-434. https://doi.org/10.1146/annurev.pathol.1.110304.100218