title: Mitochondrial biogenesis: which part of "NO" do we understand?
abstract: A recent paper by Nisoli et al. [1] provides the first evidence that elevated levels of nitric oxide (NO) stimulate mitochondrial biogenesis in a number of cell lines via a soluble guanylate-cyclase-dependent signaling pathway that activates PGC1alpha (peroxisome proliferator-activated receptor gamma coactivator-1alpha), a master regulator of mitochondrial content. These results raise intriguing possibilities for a role of NO in modulating mitochondrial content in response to physiological stimuli such as exercise or cold exposure. However, whether this signaling cascade represents a widespread mechanism by which mammalian tissues regulate mitochondrial content, and how it might integrate with other pathways that control PGC1alpha expression, remain unclear.
authors.affiliation: Montreal Neurological Institute and Department of Human Genetics, McGill University, Montreal, Quebec, Canada.
authors.forename: Scot C
authors.initials: SC
authors.lastname: Leary
authors.forename: Eric A
authors.initials: EA
authors.lastname: Shoubridge
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002460:Cell Line; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D008954:Models, Biological; D009569:Nitric Oxide / Q000502:physiology*; D020033:Protein Isoforms; D015398:Signal Transduction; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D020033:Protein Isoforms; D014157:Transcription Factors; C111264:peroxisome-proliferator-activated receptor-gamma coactivator-1; D009569:Nitric Oxide; D000255:Adenosine Triphosphate