{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["You JS"],"funding":["National Center for Advancing Translational Sciences","NIAMS NIH HHS","NIGMS NIH HHS","Muscular Dystrophy Association","National Science Foundation"],"pagination":["1880-1893"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10401546"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(4)"],"pubmed_abstract":["<h4>Background</h4>Duchenne muscular dystrophy (DMD), caused by dystrophin deficiency, leads to progressive and fatal muscle weakness through yet-to-be-fully deciphered molecular perturbations. Emerging evidence implicates RhoA/Rho-associated protein kinase (ROCK) signalling in DMD pathology, yet its direct role in DMD muscle function, and related mechanisms, are unknown.<h4>Methods</h4>Three-dimensionally engineered dystrophin-deficient mdx skeletal muscles and mdx mice were used to test the role of ROCK in DMD muscle function in vitro and in situ, respectively. The role of ARHGEF3, one of the RhoA guanine nucleotide exchange factors (GEFs), in RhoA/ROCK signalling and DMD pathology was examined by generating Arhgef3 knockout mdx mice. The role of RhoA/ROCK signalling in mediating the fun"],"journal":["Journal of cachexia, sarcopenia and muscle"],"pubmed_title":["RhoA/ROCK signalling activated by ARHGEF3 promotes muscle weakness via autophagy in dystrophic mdx mice."],"pmcid":["PMC10401546"],"funding_grant_id":["R56 AR048914","R01GM089771","R01 GM089771","#CBET0939511","#1830881","#864137","R56AR048914"],"pubmed_authors":["Lee S","Chen J","Kim Y","You JS","Bashir R"],"additional_accession":[]},"is_claimable":false,"name":"RhoA/ROCK signalling activated by ARHGEF3 promotes muscle weakness via autophagy in dystrophic mdx mice.","description":"<h4>Background</h4>Duchenne muscular dystrophy (DMD), caused by dystrophin deficiency, leads to progressive and fatal muscle weakness through yet-to-be-fully deciphered molecular perturbations. Emerging evidence implicates RhoA/Rho-associated protein kinase (ROCK) signalling in DMD pathology, yet its direct role in DMD muscle function, and related mechanisms, are unknown.<h4>Methods</h4>Three-dimensionally engineered dystrophin-deficient mdx skeletal muscles and mdx mice were used to test the role of ROCK in DMD muscle function in vitro and in situ, respectively. The role of ARHGEF3, one of the RhoA guanine nucleotide exchange factors (GEFs), in RhoA/ROCK signalling and DMD pathology was examined by generating Arhgef3 knockout mdx mice. The role of RhoA/ROCK signalling in mediating the fun","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2025-04-20T03:14:52.726Z","creation":"2025-04-20T03:14:52.726Z"},"accession":"S-EPMC10401546","cross_references":{"pubmed":["37311604"],"doi":["10.1002/jcsm.13278"]}}