Cellular Senescence and the Biology of Aging, Disease, and Frailty

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Population aging simultaneously highlights the remarkable advances in science, medicine, and public policy, and the formidable challenges facing society. Indeed, aging is the primary risk factor for many of the most common chronic diseases and frailty, which result in profound social and economic costs. Population aging also reveals an opportunity, i.e. interventions to disrupt the fundamental biology of aging could significantly delay the onset of age-related conditions as a group, and, as a result, extend the healthy life span, or health span . There is now considerable evidence that cellular senescence is an underlying mechanism of aging and age-related conditions. Cellular senescence is a process in which cells lose the ability to divide and damage neighboring cells by the factors they secrete, collectively referred to as the senescence-associated secretory phenotype (SASP). Herein, we discuss the concept of cellular senescence, review the evidence that implicates cellular senescence and SASP in age-related deterioration, hyperproliferation, and inflammation, and propose that this underlying mechanism of aging may play a fundamental role in the biology of frailty.

Original languageEnglish (US)
Pages (from-to)11-18
Number of pages8
JournalNestle Nutrition Institute Workshop Series
Volume83
DOIs
StatePublished - 2015

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Cell Aging
Cell Biology
Biological Sciences
Phenotype
phenotype
economic costs
public policy
Public Policy
chronic diseases
Age of Onset
Population
medicine
Chronic Disease
risk factors
inflammation
deterioration
Economics
Medicine
cells
Inflammation

ASJC Scopus subject areas

  • Food Science
  • Pediatrics, Perinatology, and Child Health
  • Nutrition and Dietetics

Cite this

Cellular Senescence and the Biology of Aging, Disease, and Frailty. / LeBrasseur, Nathan K; Tchkonia, Tamara; Kirkland, James L.

In: Nestle Nutrition Institute Workshop Series, Vol. 83, 2015, p. 11-18.

Research output: Contribution to journalArticle

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