Summary by Dr Alice Rannou

Short title: Targeting myofiber maturation to enhance muscle regeneration in Duchenne muscular dystrophy

Publication

https://www.nature.com/articles/s41467-026-72824-8

Tang, W., Lin, B., Jin, M. et al. ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD). Nat Commun (2026). https://doi.org/10.1038/s41467-026-72824-8

Summary

ANXA11 as a disease modifier in Duchenne muscular dystrophy. Duchenne muscular dystrophy (DMD) is characterised not only by progressive muscle degeneration, but also by impaired regenerative myofiber maturation. In our recent study, published in Nature Communications: "ANXA11 Suppression Restores Muscular Function in the mdx Mouse Model of Duchenne Muscular Dystrophy" DOI: 10.1038/s41467-026-72824-8, we identified ANXA11 as a key regulator of regenerative myofibre maturation in DMD. We found that ANXA11 is highly upregulated in fragile MYH3-positive regenerating fibres in both DMD patients and mdx mice. Suppression of ANXA11 promotes regenerative myofibre maturation, restores downstream mTOR–S6 signalling activity, and improves muscle function in dystrophic muscle. Our findings further suggest that chronic dystrophic regeneration is associated with an "uncoupling" of mTOR signalling, characterised by persistent upstream activation but impaired downstream S6 signalling, and that ANXA11 contributes to this pathological state. Take-home messages: DMD progression involves defective regenerative maturation beyond membrane instability. ANXA11 contributes to chronic regenerative failure through dysregulated mTOR–S6 signalling. Restoring regenerative quality may represent a complementary therapeutic strategy for Duchenne muscular dystrophy.

This study moves beyond the classical view of DMD as solely a structural dystrophin defect and focuses on regenerative dysfunction as a therapeutic opportunity. By identifying ANXA11 as a regulator of myofibre maturation, the authors open a new avenue for combination therapies aimed at enhancing muscle repair in dystrophic muscle.

About the author

Dr Wen Tang is currently a postdoctoral research associate in the Department of Chemistry at the University of Oxford. She obtained her PhD from the School of Medicine at Zhejiang University under the supervision of Dr Zhen Zhong. Her doctoral research focused on Duchenne muscular dystrophy (DMD) and the molecular mechanisms underlying skeletal muscle regeneration.

About the reviewer

Dr Alice Rannou is currently a postdoctoral researcher at the TaRGeT laboratory (UMR 1089) at Nantes Université (France), where she works on neuromuscular gene therapy approaches for skeletal muscle diseases under the supervision of Dr Nicolas Wein. She obtained her PhD in France, where her research focused on stem cell–based therapeutic strategies for myocardial infarction. She subsequently completed a postdoctoral fellowship at Cedars-Sinai Medical Center (Los Angeles, USA) in the laboratory of Dr Eduardo Marbán, where she specialised in translational and preclinical research in cardiac and skeletal muscle diseases, including Duchenne muscular dystrophy.