Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention.
dc.contributor.author | Galkin, A | |
dc.contributor.author | Moncada, Salvador | |
dc.date.accessioned | 2017-05-12T12:41:09Z | |
dc.date.available | 2017-05-12T12:41:09Z | |
dc.date.issued | 2017-04-06 | |
dc.identifier.citation | Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention. 2017, 7 (2):20160104 Interface Focus | en |
dc.identifier.issn | 2042-8898 | |
dc.identifier.pmid | 28382200 | |
dc.identifier.doi | 10.1098/rsfs.2016.0104 | |
dc.identifier.uri | http://hdl.handle.net/10541/620361 | |
dc.description.abstract | In recent years, there have been significant advances in our understanding of the functions of mitochondrial complex I other than the generation of energy. These include its role in generation of reactive oxygen species, involvement in the hypoxic tissue response and its possible regulation by nitric oxide (NO) metabolites. In this review, we will focus on the hypoxic conformational change of this mitochondrial enzyme, the so-called active/deactive transition. This conformational change is physiological and relevant to the understanding of certain pathological conditions including, in the cardiovascular system, ischaemia/reperfusion (I/R) damage. We will discuss how complex I can be affected by NO metabolites and will outline some potential mitochondria-targeted therapies in I/R damage. | |
dc.language.iso | en | en |
dc.rights | Archived with thanks to Interface focus | en |
dc.title | Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention. | en |
dc.type | Article | en |
dc.contributor.department | Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, 401 East 61st Street, 5th floor, New York, NY 10065, USA | en |
dc.identifier.journal | Interface Focus | en |
html.description.abstract | In recent years, there have been significant advances in our understanding of the functions of mitochondrial complex I other than the generation of energy. These include its role in generation of reactive oxygen species, involvement in the hypoxic tissue response and its possible regulation by nitric oxide (NO) metabolites. In this review, we will focus on the hypoxic conformational change of this mitochondrial enzyme, the so-called active/deactive transition. This conformational change is physiological and relevant to the understanding of certain pathological conditions including, in the cardiovascular system, ischaemia/reperfusion (I/R) damage. We will discuss how complex I can be affected by NO metabolites and will outline some potential mitochondria-targeted therapies in I/R damage. |