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.
|主出版物子標題||Oxidative Stress and Dietary Antioxidants|
|出版狀態||Published - 2014 三月|
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