Oxidative Stress and Frailty: A Closer Look at the Origin of a Human Aging Phenotype

I. Chien Wu, Chao A. Hsiung, Chih Cheng Hsu, Xi Zhang Lin

Research output: Chapter in Book/Report/Conference proceedingChapter

6 Citations (Scopus)

Abstract

Frailty is an important health problem for older adults. Its clinical significance is increasingly being demonstrated and recognized. The pathogenesis of frailty involves insulin resistance, inflammation, sarcopenia, adiposity, age-related hormone decline, and nervous system dysfunction. What remains unclear is how these abnormalities of multiple physiologic systems occur as we age. The answer may lie in the increased oxidative stress that occurs during aging. Correlative human studies using different markers of oxidative stress consistently showed that increased oxidative stress independently predicts frailty. Transgenic mice with high oxidative stress display pathologies and phenotypes resembling those of frailty. Oxidative stress can cause frailty by the following cellular mechanisms: mitochondrial dysfunction; damage to proteins critical for maintaining homeostasis and muscle function; endoplasmic reticulum (ER) stress; cellular apoptosis; cellular senescence; and abnormal cellular signaling. Oxidative stress and its downstream cellular pathogenic pathways may offer the targets for prevention and intervention strategies against frailty. Further studies are required in this field.

Original languageEnglish
Title of host publicationAging
Subtitle of host publicationOxidative Stress and Dietary Antioxidants
PublisherElsevier Inc.
Pages3-14
Number of pages12
ISBN (Print)9780124059337
DOIs
Publication statusPublished - 2014 Mar

All Science Journal Classification (ASJC) codes

  • General Dentistry
  • General Medicine

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