Loss of a regulatory protein worsened bone loss in mice
Experiments found that mice lacking SIRT5, a protein that modifies other proteins, had poorer bone formation and more severe bone loss than normal mice.
Multicenter
Limit: The abstract omits sample sizes, making the reliability of the bone-loss result difficult to assess
Edited by Boris Djordjevic · AgingResearch.News
Animal experiments examined naturally aged mice and mice engineered to lack SIRT5 or PRMT6, two regulatory proteins. Researchers also studied primary osteoblasts—bone-forming cells—grown in the lab under repeated cell division or chemically induced stress.
Mice lacking SIRT5 had more severe deterioration of the spongy bone inside bones and poorer bone formation than normal mice. Losing PRMT6 lowered SIRT5 levels and produced similar bone deterioration. Increasing SIRT5 production alleviated bone loss in mice. In cells grown in the lab, increasing SIRT5 reduced the buildup of R-loops, structures in which RNA binds to DNA. It also reduced signs of senescence, a state in which cells stop dividing, induced by oxidative stress or loss of PRMT6.
Why it matters
Declining bone-forming cell function contributes to skeletal aging. The authors suggest that targeting this protein pathway may offer a strategy for preventing age-related osteoporosis.
Caveats
These experiments involved mice and cells grown in the lab, not people. The abstract does not report sample sizes or the size of the bone-loss benefit.
