Sulfur molecule shields muscle repair protein from age-related damage

Kyushu University researchers said a sulfur-based molecule called LASSS more than doubled the strength of HGF, the hepatocyte growth factor that helps activate muscle repair, by making the protein more resistant to age-related damage. The study, led by Professor Ryuichi Tatsumi, was published in Scientific Reports and announced by the university on July 24, 2026.

The finding matters because it targets a fragile step in aging muscle biology: keeping a repair signal intact long enough to do its job. HGF sits upstream of muscle regeneration, so protecting it from the chemical wear that comes with age could help preserve the body’s ability to respond after injury or chronic decline. Kyushu University framed the work as a potential future treatment avenue for age-related muscle loss in humans and pets, but the result itself remains a molecular advance rather than a therapy.

That focus lines up with how sarcopenia behaves in the body. News-Medical noted that skeletal muscle is among the first tissues to decline with age, and that decline can bring weakness, scarring, fat accumulation inside muscle and loss of fast-twitch fibers, the fibers needed for quick, powerful movement. In that setting, a compound that stabilizes HGF does not rebuild muscle on its own, but it offers a new way to think about preserving the repair machinery that aging muscle depends on.

The Kyushu work also fits a longer research arc at the university. A 2021 Kyushu University-associated epidemiology study in the Hisayama population examined the prevalence and mortality of sarcopenia in community-dwelling older Japanese adults, grounding the question in real aging demographics in Hisayama, Japan. The university has also previously posted research on developing an antibody to combat age-related muscle atrophy.

For protein scientists, LASSS is notable less as a finished intervention than as a mechanism-forward lead: a sulfur-based compound that protects a repair protein before it fails. If that strategy can be extended beyond the bench, it could eventually influence research on frailty, sarcopenia and other age-related muscle decline, where maintaining protein function may matter as much as replacing what has already been lost.