Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-11-27
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1553-4006
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
405-34
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Calcium in cell injury and death.
pubmed:affiliation
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912, USA. zdong@mcg.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural