Health
Combination of exercise and cell aging drugs can help people with chronic inflammatory myopathy
Exercise can only improve the intensity of myogenic degenerative diseases when certain types of muscle cells age, reports researchers at Hokkaido University and colleagues at Sapporo Medical University in Japan. Their findings using mouse models have been published in journals Natural communication.
Idiopathic inflammatory myopathy is a rare disease that causes muscle weakness, inflammation, and fibrosis. In addition to drugs, exercise is a powerful treatment for some patients. However, in the case of chronic inflammatory myopathy, exercise can actually trigger muscle inflammation and fibrosis. Scientists have wanted to understand why the exercise benefits some myopathy but not others.
Chikenji Takako S. Chikenji of Hokkaido University has collaborated with Yuki Saito and Minoko Fujimiya of Sapporo Medical University in Japan to determine the type of muscle cells called muscle adipocyte progenitor cells (FAP) according to the type of myopathy. We investigated why they respond differently to exercise. These cells are important regulators of muscle stem cells required for regeneration.
They investigated what happens when mice with myopathy exercise. In mice with acute muscle injury simulating idiopathic inflammatory myopathy, FAP increased initially but returned to preinjury levels after 7 days. These FAPs eventually died and were cleared by immune cells that eat cells called phagocytes. In mice with chronic inflammatory myopathy, FAP continued to grow for 14 days and was resistant to cell death and immune cell clearance.
Upon further investigation, the team found that FAP in mice with acute muscle injury showed strong signs of aging after exercise, but did not in mice with chronic inflammatory myopathy. They also found that normal FAP induced muscle cell regeneration following acute muscle injury, but not FAP lacking a cellular senescence inducer. These results summarize the aging of FAP after requiring exercise to establish a state of regenerative inflammation that induces muscle regeneration.
In addition, the combination of drugs that induce exercise and cell senescence restored FAP aging in mice with chronic inflammatory myopathy and improved muscle function and regeneration.
Our findings indicate that exercise leads to muscle degeneration in chronic inflammatory myopathy. This is because FAP accumulates when aging fails. Pharmacological induction of FAP aging dramatically improved the therapeutic effect of exercise in mice with chronic myopathy. Further research is needed to investigate whether this strategy can be used to treat this condition in humans. “
Takako Chikenji, Hokkaido University
Source:
Journal reference:
Yu Saito other (2020) Exercise enhances skeletal muscle regeneration by promoting the aging of fibrolipid preadipocytes. Natural communication. doi.org/10.1038/s41467-020-14734-x.
Posted in: Cell biology
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