NF-κB in aging and disease

Jeremy S. Tilstra, Cheryl L. Clauson, Laura J. Niedernhofer, Paul D. Robbins

Research output: Contribution to journalReview article

156 Scopus citations

Abstract

Stochastic damage to cellular macromolecules and organelles is thought to be a driving force behind aging and associated degenerative changes. However, stress response pathways activated by this damage may also contribute to aging. The IKK/NF-κB signaling pathway has been proposed to be one of the key mediators of aging. It is activated by genotoxic, oxidative, and inflammatory stresses and regulates expression of cytokines, growth factors, and genes that regulate apoptosis, cell cycle progression, cell senescence, and inflammation. Transcriptional activity of NF-κB is increased in a variety of tissues with aging and is associated with numerous age-related degenerative diseases including Alzheimer's, diabetes and osteoporosis. In mouse models, inhibition of NF-κB leads to delayed onset of age-related symptoms and pathologies. In addition, NF-κB activation is linked with many of the known lifespan regulators including insulin/IGF-1, FOXO, SIRT, mTOR, and DNA damage. Thus NF-κB represents a possible therapeutic target for extending mammalian healthspan.

Original languageEnglish (US)
Pages (from-to)449-465
Number of pages17
JournalAging and Disease
Volume2
Issue number6
StatePublished - Jan 1 2011
Externally publishedYes

Keywords

  • Aging
  • Inflammation
  • NF-κB
  • Senescence

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    Tilstra, J. S., Clauson, C. L., Niedernhofer, L. J., & Robbins, P. D. (2011). NF-κB in aging and disease. Aging and Disease, 2(6), 449-465.