Protein oxidative damage at the crossroads of cellular senescence, aging, and age-related diseases.

ABSTRACT: Protein damage mediated by oxidation, protein adducts formation with advanced glycated end products and with products of lipid peroxidation, has been implicated during aging and age-related diseases, such as neurodegenerative diseases. Increased protein modification has also been described upon replicative senescence of human fibroblasts, a valid model for studying aging in vitro. However, the mechanisms by which these modified proteins could impact on the development of the senescent phenotype and the pathogenesis of age-related diseases remain elusive. In this study, we performed in silico approaches to evidence molecular actors and cellular pathways affected by these damaged proteins. A database of proteins modified by carbonylation, glycation, and lipid peroxidation products during agi

SUBMITTER: Baraibar MA 

PROVIDER: S-EPMC3483731 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature