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Protection from oxidative stress by enhanced glycolysis; a possible mechanism of cellular immortalization

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dc.contributor.authorKondoh, H.es
dc.contributor.authorLleonart, M.E.es
dc.contributor.authorBernard, D.
dc.contributor.authorGil, J.
dc.date.accessioned2012-05-21T12:08:10Z
dc.date.available2012-05-21T12:08:10Z
dc.date.issued2007
dc.description.abstractReactive oxygen species (ROS) play a crucial role not only in the physiological signal transduction but also in the pathogenesis of several human diseases such as atherosclerosis, neurodegenerative diseases, metabolic disorders, aging or cancer amongst others. Oxidative stress is also responsible for cellular and organism senescence, in accordance with what Harman initially proposed in the free radical theory of aging. Recent findings support the notion that protection from oxidative stress can increase life span significantly. We reported that enhanced glycolysis could modulate cellular life span with reduction of oxidative stress. Moreover, the tumor suppressor gene p53 controls post-transcriptionally the level of the glycolytic enzyme, phosphoglycerate mutase (PGM). As enhanced glycolysis is a distinctive and prominent feature of cancer cells (termed the Warburg effect), our findings disclosed a novel aspect of the Warburg effect: the connection between senescence and oxidative stress.es
dc.formatapplication/pdfes
dc.format.extent6es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/27526
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectGlycolysises
dc.subjectOxidative stresses
dc.subject.other61 - Medicinaes
dc.titleProtection from oxidative stress by enhanced glycolysis; a possible mechanism of cellular immortalizationes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.22, nº 1 (2007)