Cellular mechanisms of complex I-associated pathology.
Biochem Soc Trans
; 47(6): 1963-1969, 2019 12 20.
Article
en En
| MEDLINE
| ID: mdl-31769488
ABSTRACT
Mitochondria control vitally important functions in cells, including energy production, cell signalling and regulation of cell death. Considering this, any alteration in mitochondrial metabolism would lead to cellular dysfunction and the development of a disease. A large proportion of disorders associated with mitochondria are induced by mutations or chemical inhibition of the mitochondrial complex I - the entry point to the electron transport chain. Subunits of the enzyme NADH ubiquinone oxidoreductase, are encoded by both nuclear and mitochondrial DNA and mutations in these genes lead to cardio and muscular pathologies and diseases of the central nervous system. Despite such a clear involvement of complex I deficiency in numerous disorders, the molecular and cellular mechanisms leading to the development of pathology are not very clear. In this review, we summarise how lack of activity of complex I could differentially change mitochondrial and cellular functions and how these changes could lead to a pathology, following discrete routes.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Complejo I de Transporte de Electrón
Tipo de estudio:
Risk_factors_studies
Límite:
Humans
Idioma:
En
Revista:
Biochem Soc Trans
Año:
2019
Tipo del documento:
Article
País de afiliación:
Reino Unido