Inhibiting a signaling pathway protects microgravity-exposed mice from losing muscle and bone mass, a study finds. The simultaneous loss of bone and skeletal muscle is a major challenge facing astronauts on long-term missions, as well as individuals with disuse atrophy. One potential preventive or therapeutic strategy is to target the myostatin/activin A signaling pathway, a cellular mechanism that regulates bone density and skeletal muscle mass. Se-Jin Lee and colleagues tested this strategy in mice exposed to microgravity at the International Space Station for 33 days, compared with mice maintained on Earth. The authors inhibited myostatin/activin A signaling through injections of the activin type IIB (ACVR2B) decoy receptor. Treatment with the ACVR2B receptor led to similar increases in muscle and bone mass in microgravity-exposed and Earth-bound mice, when compared with untreated control mice. Moreover, mice treated with the ACVR2B receptor after returning to Earth showed enhanced recovery of muscle mass, compared with untreated control mice that had returned from microgravity. Taken together, the findings suggest that inhibiting myostatin/activin A signaling could simultaneously protect against muscle and bone loss during spaceflight and promote recovery of muscle and bone mass after return to Earth, according to the authors.
Article #20-14716: "Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight," by Se-Jin Lee et al.
MEDIA CONTACT: Se-Jin Lee, The Jackson Laboratory for Genomic Medicine, Farmington, CT; tel: 443-520-9860; e-mail: se-jin.Lee@jax.org
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Journal
Proceedings of the National Academy of Sciences