期刊
CELL
卷 146, 期 5, 页码 682-695出版社
CELL PRESS
DOI: 10.1016/j.cell.2011.07.030
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资金
- Ligue Nationale contre le Cancer (Equipes labellisee)
- Agence Nationale pour la Recherche
- AXA Chair for Longevity Research
- European Commission (Apo-Sys, ArtForce, ChemoRes, Apop-Train)
- Fondation Bettencourt-Schueller
- Fondation pour la Recherche Medicale
- LabEx Immuno-Oncology
- Institut National du Cancer
- Canceropole Ile-de-France
- Wellcome Trust
- Wellcome Trust/Medical Research Council Strategic Award on Neurodegenerative Diseases
- Medical Research Council
- National Institute for Health Research Biomedical Research Centre at Addenbrooke's Hospital
- Medical Research Council [MC_G1000734, G0600194] Funding Source: researchfish
- MRC [G0600194, MC_G1000734] Funding Source: UKRI
Genetic inhibition of autophagy induces degenerative changes in mammalian tissues that resemble those associated with aging, and normal and pathological aging are often associated with a reduced autophagic potential. Pharmacological or genetic manipulations that increase life span in model organisms often stimulate autophagy, and its inhibition compromises the longevity-promoting effects of caloric restriction, Sirtuin 1 activation, inhibition of insulin/insulin growth factor signaling, or the administration of rapamycin, resveratrol, or spermidine. Here, we discuss the probable cause and effect relationship between perturbed autophagy and aging, as well as possible molecular mechanisms that may mediate the anti-aging effects of autophagy.
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