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New research shows that muscle decline caused by aging and certain diseases could be significantly slowed down by ending a chain reaction that damages cells.
The study revealed the then-unknown steps by which the dysfunction of mitochondria – the so-called "central" cells – harms muscle health and leads to atrophy (dieback).
The research team of Exeter and Nottingham Universities (UK) and Tohoku University in Japan showed that the inhibition of various stages of this process suppressed Muscular atrophy.
The research was conducted on a worm species called Caenorhabditis elegans – recently used in a study of the muscles of the International Space Station because their muscle cells resemble those of humans.
Mitochondrial dysfunction is a key feature of many muscle diseases, but treatments are currently limited.
Our research shows that mitochondrial dysfunction causes calcium build-up in cells, which in turn activates the enzymes that degrade collagen.
Collagen is essential for structuring the outside of cells. As a result, the breakdown of collagen destabilizes the muscle.
In this study, we used experimental drugs to inhibit collagen-degrading enzymes – and the results show this decrease in muscle decline caused by dysfunctional mitochondria.
We found the same effect in worms used to model Duchenne muscular dystrophy, which causes severe muscle weakness. "
Timothy Etheridge, University of Exeter
Further research is needed, but the results suggest new therapies to delay muscle atrophy caused by aging and conditions such as Duchenne muscular dystrophy.
Source:
University of Exeter
Journal reference:
Etheridge, T. et al. (2019) Mitochondrial dysfunction causes Ca2+ muscle overload and degradation of ECM induced by muscle degradation in C. elegans. FASEB Journal. doi.org/10.1096/fj.201802298R.
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