Researchers at Umeå University in Sweden have identified that boosting the expression of a gene known as fhl2b can slow the breakdown of muscle fibers in muscular dystrophy. The findings were published in Nature Communications.
Earlier work showed that increasing fhl2b expression in the eye muscles of zebrafish affected by muscular dystrophy correlated with preserved muscle integrity. Muscular dystrophy is a broad family of hereditary diseases marked by progressive weakness and degeneration of skeletal muscles, leading to reduced muscle mass and function. In those studies, heightened fhl2b activity did not coincide with muscle deterioration, suggesting a protective role for the gene in muscle tissue.
To probe this possibility further, the researchers enhanced fhl2b expression across all muscle tissues in zebrafish models of Duchenne muscular dystrophy, a severe form of the disease. The intervention yielded encouraging results: the fish maintained healthier muscle mass and endured longer lifespans compared with untreated counterparts. This indicates that fhl2b upregulation can influence muscle maintenance even in the presence of a serious dystrophic condition.
The scientists indicate that these results could pave the way for new treatment approaches for muscular dystrophy that hinge on manipulating fhl2b activity. However, they also emphasize the need for additional research to determine whether similar strategies could be safely and effectively translated to human patients.
In related work, researchers have explored common biological mechanisms linked to schizophrenia and aging, underscoring a broader interest in shared pathways that influence brain and muscle biology and overall health outcomes.