Rodriguez-Outeiriño, LaraHernandez-Torres, FranciscoRamirez de Acuña, FelicitasRastrojo, AlbertoCreus, CarlotaCarvajal, AlejandraSalmeron, LuisMontolio, MarisolSoblechero-Martin, PatriciaArechavala-Gomeza, VirginiaFranco, DiegoAranega, Amelia Eva2023-05-032023-05-032022-08-202162-2531http://hdl.handle.net/10668/22463Satellite cells (SCs), muscle stem cells, display functional heterogeneity, and dramatic changes linked to their regenerative capabilities are associated with muscle-wasting diseases. SC behavior is related to endogenous expression of the myogenic transcription factor MYF5 and the propensity to enter into the cell cycle. Here, we report a role for miR-106b reinforcing MYF5 inhibition and blocking cell proliferation in a subset of highly quiescent SC population. miR-106b down-regulation occurs during SC activation and is required for proper muscle repair. In addition, miR-106b is increased in dystrophic mice, and intramuscular injection of antimiR in injured mdx mice enhances muscle regeneration promoting transcriptional changes involved in skeletal muscle differentiation. miR-106b inhibition promotes the engraftment of human muscle stem cells. Furthermore, miR-106b is also high in human dystrophic muscle stem cells and its inhibition improves intrinsic proliferative defects and increases their myogenic potential. This study demonstrates that miR-106b is an important modulator of SC quiescence, and that miR-106b may be a new target to develop therapeutic strategies to promote muscle regeneration improving the regenerative capabilities of injured dystrophic muscle.enAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/MT: Non-coding RNAsmiR-106bmuscle regenerationmuscular dystrophysatellite cellstemnessresearch article36159592open access10.1016/j.omtn.2022.08.025PMC9463180http://www.cell.com/article/S2162253122002244/pdfhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9463180/pdf