AI Article Synopsis
- Aging causes skeletal muscle to accumulate oxidative damage and intramyocellular lipid droplets (IMLDs), but the specific factors influencing these changes are not well understood.
- Researchers found that the lipase ATGL, which breaks down fats, declines significantly with aging, leading to an increase in lipid droplets and oxidative damage in muscle cells.
- The study suggests that ATGL plays a crucial role in muscle cell protection against oxidative stress and inflammation, positioning it as a potential target for therapies aimed at combating muscle decline associated with aging.
Article Abstract
During aging skeletal muscle shows an accumulation of oxidative damage as well as intramyocellular lipid droplets (IMLDs). However, although the impact of these modifications on muscle tissue physiology is well established, the direct effectors critical for their occurrence are poorly understood. Here we show that during aging the main lipase of triacylglycerols, ATGL, significantly declines in gastrocnemius and its downregulation in C2C12 myoblast leads to the accumulation of lipid droplets. Indeed, we observed an increase of oxidative damage to proteins in terms of carbonylation, S-nitrosylation and ubiquitination that is dependent on a defective antioxidant cell response mediated by ATGL-PPARα-PGC-1α. Overall our findings describe a pivotal role for ATGL in the antioxidant/anti-inflammatory response of muscle cells highlighting this lipase as a therapeutic target for fighting the progressive decline in skeletal muscle mass and strength.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029607 | PMC |
| http://dx.doi.org/10.18632/oncotarget.8552 | DOI Listing |
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