Difference between revisions of "Johnson 2013 Trends Endocrinol Metab"
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{{Publication | {{Publication | ||
|title=Johnson ML, Robinson MM, Nair KS (2013) Skeletal muscle aging and the mitochondrion. Trends Endocrinol Metab | |title=Johnson ML, Robinson MM, Nair KS (2013) Skeletal muscle aging and the mitochondrion. Trends Endocrinol Metab 24: 247-256 | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23375520 PMID: 23375520] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/23375520 PMID: 23375520] | ||
|authors=Johnson ML, Robinson MM, Nair KS | |authors=Johnson ML, Robinson MM, Nair KS | ||
Revision as of 13:38, 31 May 2013
| Johnson ML, Robinson MM, Nair KS (2013) Skeletal muscle aging and the mitochondrion. Trends Endocrinol Metab 24: 247-256 |
Johnson ML, Robinson MM, Nair KS (2013) Trends Endocrinol Metab
Abstract: Decline in human muscle mass and strength (sarcopenia) is a hallmark of the aging process. A growing body of research in the areas of bioenergetics and protein turnover has placed the mitochondria at the center of this process. It is now clear that, unless an active lifestyle is rigorously followed, skeletal muscle mitochondrial decline occurs as humans age. Increasing research on mitochondrial biology has elucidated the regulatory pathways involved in mitochondrial biogenesis, many of which are potential therapeutic targets, and highlight the beneficial effects of vigorous physical activity on skeletal muscle health for an aging population. • Keywords: Aging, Sarcopenia
• O2k-Network Lab: US MN Rochester Nair KS
Labels:
Stress:Aging; Senescence"Aging; Senescence" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Skeletal muscle
HRR: Oxygraph-2k
