4.8 Review

Autophagy and Aging

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

  1. Ligue Nationale contre le Cancer (Equipes labellisee)
  2. Agence Nationale pour la Recherche
  3. AXA Chair for Longevity Research
  4. European Commission (Apo-Sys, ArtForce, ChemoRes, Apop-Train)
  5. Fondation Bettencourt-Schueller
  6. Fondation pour la Recherche Medicale
  7. LabEx Immuno-Oncology
  8. Institut National du Cancer
  9. Canceropole Ile-de-France
  10. Wellcome Trust
  11. Wellcome Trust/Medical Research Council Strategic Award on Neurodegenerative Diseases
  12. Medical Research Council
  13. National Institute for Health Research Biomedical Research Centre at Addenbrooke's Hospital
  14. Medical Research Council [MC_G1000734, G0600194] Funding Source: researchfish
  15. MRC [G0600194, MC_G1000734] Funding Source: UKRI

向作者/读者索取更多资源

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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