Ion transporters and ischemic mitochondrial dysfunction.
Cell Adh Migr
; 3(1): 94-8, 2009.
Article
en En
| MEDLINE
| ID: mdl-19276659
Ischemia-induced ionic imbalance leads to the activation of numerous events including mitochondrial dysfunction and eventual cell death. Dysregulation of mitochondrial Ca(2+) (Ca(2+)(m)) plays a critical role in cell damage under pathological conditions including traumatic brain injury and stroke. High Ca(2+)(m) levels can induce the persistent opening of the mitochondrial permeability transition pore and trigger mitochondrial membrane depolarization, Ca(2+) release, cessation of oxidative phosphorylation, matrix swelling and eventually outer membrane rupture with release of cytochrome c and other apoptogenic proteins. Thus, the dysregulation of mitochondrial Ca(2+) homeostasis is now recognized to play a crucial role in triggering mitochondrial dysfunction and subsequent apoptosis. Recent studies show that some secondary active transport proteins, such as Na(+)-dependent chloride transporter and Na(+)/Ca(2+) exchanger, contribute to ischemia-induced dissipation of ion homeostasis including Ca(2+)(m).
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas de Transporte de Membrana
/
Isquemia
/
Mitocondrias
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Cell Adh Migr
Año:
2009
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos