Signal transduction, ageing and disease

Lei Zhang, Matthew J. Yousefzadeh, Yousin Suh, Laura J. Niedernhofer, Paul D. Robbins

Research output: Chapter in Book/Report/Conference proceedingChapter

33 Scopus citations

Abstract

Ageing is defined by the loss of functional reserve over time, leading to a decreased tissue homeostasis and increased age-related pathology. The accumulation of damage including DNA damage contributes to driving cell signaling pathways that, in turn, can drive different cell fates, including senescence and apoptosis, as well as mitochondrial dysfunction and inflammation. In addition, the accumulation of cell autonomous damage with time also drives ageing through non-cell autonomous pathways by modulation of signaling pathways. Interestingly, genetic and pharmacologic analysis of factors able to modulate lifespan and healthspan in model organisms and even humans have identified several key signaling pathways including IGF-1, NF-κB, FOXO3, mTOR, Nrf-2 and sirtuins. This review will discuss the roles of several of these key signaling pathways, in particular NF-κB and Nrf2, in modulating ageing and age-related diseases.

Original languageEnglish (US)
Title of host publicationSubcellular Biochemistry
PublisherSpringer New York
Pages227-247
Number of pages21
Volume91
DOIs
StatePublished - Mar 20 2019

Publication series

NameSub-cellular biochemistry
PublisherPlenum Publishers
ISSN (Print)0306-0225

Bibliographical note

Funding Information:
Acknowledgements This work was supported by the NIH grants P01-AG043376 (PDR, LJN), U19-AG056278 (PDR, LJN, YS) and the Glenn/AFAR (LJN).

Publisher Copyright:
© 2019, Springer Nature Singapore Pte Ltd.

Keywords

  • Age-related disease
  • Apoptosis
  • Inflammation
  • NF-κB Nrf2
  • Senescence
  • Signaling pathways
  • Sirtuins
  • Aging/genetics
  • Humans
  • Signal Transduction/genetics
  • Animals
  • Cellular Senescence
  • Longevity/genetics
  • NF-E2-Related Factor 2/metabolism
  • NF-kappa B/metabolism

PubMed: MeSH publication types

  • Review
  • Journal Article

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