RT Journal Article
T1 Induction of the Mitochondrial NDUFA4L2 Protein by HIF-1α Decreases Oxygen Consumption by Inhibiting Complex I Activity
A1 Tello, Daniel
A1 Balsa, Eduardo
A1 Acosta-Iborra, Bárbara
A1 Fuertes-Yebra, Esther
A1 Elorza, Ainara
A1 Ordóñez, Ángel
A1 Corral-Escariz, María
A1 Soro, Inés
A1 López-Bernardo, Elia
A1 Perales-Clemente, Ester
A1 Martínez Ruiz, Antonio
A1 Enríquez, José Antonio
A1 Aragonés, Julián
A1 Cadenas, Susana
A1 Landázuri, Manuel O.
AB The fine regulation of mitochondrial function has proved to be an essential metabolic adaptation to fluctuations in oxygen availability. During hypoxia, cells activate an anaerobic switch that favors glycolysis and attenuates the mitochondrial activity. This switch involves the hypoxia-inducible transcription factor-1 (HIF-1). We have identified a HIF-1 target gene, the mitochondrial NDUFA4L2 (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex, 4-like 2). Our results, obtained employing NDUFA4L2-silenced cells and NDUFA4L2 knockout murine embryonic fibroblasts, indicate that hypoxiainduced NDUFA4L2 attenuates mitochondrial oxygen consumption involving inhibition of Complex I activity, which limits the intracellular ROS production under low-oxygen conditions. Thus, reducing mitochondrial Complex I activity via NDUFA4L2 appears to be an essential element in the mitochondrial reprogramming induced by HIF-1.
SN 1550-4131
YR 2011
FD 2011-12-07
LK https://hdl.handle.net/20.500.14352/104286
UL https://hdl.handle.net/20.500.14352/104286
LA eng
NO Ministerio de Ciencia e Innovación
NO Comunidad Auto´ noma de Madrid (SAL 2006/ 0311), Metoxia Project-Health (F2 2009-222741), and Recava Network (RD 06/0014/0031) to M.O.L.; PS09/00101 and CP07/00143 to A.M.-R.; PI060701, PS09/00116, and CP08/00204 to S.C.; BFU2008-03407/BMC to J.A.; SAF2009-08007 to J.A.E.; and CSD2007-00020
DS Docta Complutense
RD 28 jul 2024