Evidence for Disruption of Autophagy in Sarcopenia

Sarcopenia is the name given to age-related loss of muscle mass and strength. Researchers here provide somewhat indirect evidence in support of defects in autophagy, a cellular housekeeping process, being involved in the development of sarcopenia. Autophagy is known to fail with age for reasons that include the accumulation of metabolic waste in cell lysosomes, the structures responsible for breaking down damaged structures to recycle their component parts. Improved autophagy shows up in many of the approaches demonstrated to slow aging in mammals. The practice of calorie restriction improves the state of both autophagy and sarcopenia, for example.

One should always be wary of correlations in aging, of course: aging is caused by damage, and various forms of damage and consequences build up in many tissues at a similar pace. There is no necessary reason for any two correlated aspects of aging to be directly connected simply because they are happening at the same time:

Sarcopenia is the aging-related loss of skeletal muscle mass and strength. Preventing sarcopenia is important for maintaining a high quality of life in the aged population. However, the molecular mechanism of sarcopenia has not yet been unraveled and is still a matter of debate. Determining whether the levels of autophagy-related mediators (e.g., p62/SQSTM1, LC3, etc.) in muscle change with ageing is important to understanding sarcopenia. Such information could enhance the therapeutic strategies for attenuating mammalian sarcopenia.

In previous studies, autophagic defects were detected in the sarcopenic muscle of mice, rats, and humans. However, all these studies involved only western blotting analyses of crude not cell-fractionated muscle homogenates. Thus, these data were insufficient to describe the adaptive changes in autophagy-linked molecules within sarcopenic muscle. Researchers found a marked accumulation of p62/SQSTM1 in the sarcopenic quadriceps muscle of mice using two different methods (western blotting of cell-fractionated homogenates and immunofluorescence). In contrast, the expression level of LC3, a partner of p62/SQSTM1 in autophagy progression, was not modulated. The found autophagic defect improves our understanding of the mechanism underlying sarcopenia. The researchers would like to further study this mechanism with an aim to attenuate sarcopenia by improving this autophagic defect using nutrient- and pharmaceutical-based treatments.

Link: http://www.eurekalert.org/pub_releases/2015-06/tuot-ad060515.php

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