Calcium in cell injury and death

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

Research output: Contribution to journalReview articlepeer-review

214 Scopus citations


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
StatePublished - 2006


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

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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