Key result
Wnt7a suppresses intramuscular fatty infiltration in injured mouse muscle without impairing myogenesis or inducing fibrosis.
Why the study?
Intramuscular delivery of Wnt7a stimulates muscle regeneration, but its effects on the adipogenic conversion of fibro-adipogenic progenitors remain unknown.
Does intramuscular Wnt7a prevent adipogenesis of FAPs and fatty infiltration in mice?
Does intramuscular Wnt7a prevent adipogenesis of FAPs and fatty infiltration in mice?
p-value: p=<0.05
Wnt7a may serve as a potential protein-based therapeutic for inhibiting intramuscular fatty infiltration in pathological muscle injuries or diseases.
Warrants investigation as therapy for muscle fatty infiltration; hypothesis-generating in mice and requires human validation before clinical consideration.
Intramuscular fatty infiltration in muscle injuries and diseases, caused by aberrant adipogenesis of fibro-adipogenic progenitors, negatively impacts function. Intramuscular delivery of Wnt7a offers a promising strategy to stimulate muscle regeneration but its effects on adipogenic conversion of fibro-adipogenic progenitors remain unknown. Here we show that Wnt7a inhibits adipogenesis of FAPs through the alternative Wnt-Rho-YAP/TAZ signaling that subsequently upregulates the canonical Wnt pathway. Furthermore, intramuscular injection of Wnt7a in vivo effectively suppresses fatty infiltration in mice. Our results collectively suggest Wnt7a as a potential protein-based therapeutic for inhibiting adipogenesis of FAPs and intramuscular fatty infiltration in pathological muscle injuries or diseases.
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Fu et al. (2022) studied Intramuscular fatty infiltration. Wnt7a vs. Saline was evaluated on Intramuscular fatty infiltration (perilipin-1 expression) (p=<0.05). Wnt7a effectively suppressed intramuscular fatty infiltration in a mouse model of glycerol-induced muscle injury without negatively impacting myogenesis or inducing fibrosis.
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