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dc.contributor.authorPeggion, Caterina-
dc.contributor.authorBonadio, Raphael Severino-
dc.contributor.authorStella, Roberto-
dc.contributor.authorScalabrin, Silvia-
dc.contributor.authorPasetto, Laura-
dc.contributor.authorMillino, Caterina-
dc.contributor.authorCamporeale, Laura-
dc.contributor.authorPacchioni, Beniamina-
dc.contributor.authorBonetto, Valentina-
dc.contributor.authorBertoli, Alessandro-
dc.contributor.authorCagnin, Stefano-
dc.contributor.authorMassimino, Maria Lina-
dc.date.accessioned2026-01-29T13:22:40Z-
dc.date.available2026-01-29T13:22:40Z-
dc.date.issued2025-05-30-
dc.identifier.citationPEGGION, Caterina et al. Restoration of myogenesis in ALS-myocytes through miR-26a-5p-mediated Smad4 inhibition and its impact on motor neuron development. Molecular Therapy: Nucleic Acids, v. 36, n. 3, e102581, 2025. DOI: https://doi.org/10.1016/j.omtn.2025.102581. Disponível em: https://www.sciencedirect.com/science/article/pii/S2162253125001350?via%3Dihub. Acesso em: 27 jan. 2026.pt_BR
dc.identifier.urihttp://repositorio.unb.br/handle/10482/53798-
dc.language.isoengpt_BR
dc.publisherElsevierpt_BR
dc.rightsAcesso Abertopt_BR
dc.titleRestoration of myogenesis in ALS-myocytes through miR-26a-5p-mediated Smad4 inhibition and its impact on motor neuron developmentpt_BR
dc.typeArtigopt_BR
dc.subject.keywordRNAs não-codificadorespt_BR
dc.subject.keywordEsclerose lateral amiotróficapt_BR
dc.subject.keywordDoenças neuromuscularespt_BR
dc.subject.keywordMúsculo esqueléticopt_BR
dc.rights.licenseThis is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.omtn.2025.102581pt_BR
dc.description.abstract1Amyotrophic lateral sclerosis (ALS) is the most common adult-onset paralytic disorder, characterized primarily by a progressive loss of motor neurons (MNs) in which degeneration skeletal muscle involvement has been demonstrated. Skeletal muscle is a plastic tissue that responds to insults through proliferation and differentiation of satellite cells. Skeletal muscle degeneration and regeneration are finely regulated by signals that regulate satellite cell proliferation and differentiation. It is known that satellite cell differentiation is impaired in ALS, but little is known about the involvement of microRNAs (miRNAs) and their role in intercellular communication in ALS. Here we demonstrated impaired differentiation of satellite cells derived from ALS mice related to the impairment of myogenic p38MAPK and protein kinase A (PKA)/pCREB signaling pathways that can be regulated by miR-882 and -134-5p. These miRNAs participate in autocrine signaling in association with miR-26a-5p that, secreted from wild-type (WT) and captured by ALS myoblasts, enhances ALS-related myoblast differentiation by repressing Smad4-related signals. Moreover, miR-26a-5p and -431-5p work in a paracrine way ameliorating motoneuron differentiation. These findings emphasize the need to better understand intercellular communication and its role in ALS pathogenesis and progression. They also suggest that miRNAs could be targeted or used as therapeutic agents for myofiber and MN regeneration.pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9967-2629pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4832-2776pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1462-4423pt_BR
dc.identifier.orcidhttps://orcid.org/0009-0000-3604-8792pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0319-4448pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0456-2054pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1202-0191pt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationIstituto Zooprofilattico Sperimentale delle Venezie, Department of Chemistrypt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Research Center for ALSpt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Research Center for ALSpt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Research Center for ALSpt_BR
dc.contributor.affiliationUniversity of Padova, Department of Biomedical Sciencespt_BR
dc.contributor.affiliationUniversity of Padova, Padova Neuroscience Centerpt_BR
dc.contributor.affiliationNational Research Council (CNR), Section of Padova, Neuroscience Institutept_BR
dc.contributor.affiliationUniversity of Padova, Department of Biologypt_BR
dc.contributor.affiliationUniversity of Padova, CIR-Myo Myology Centerpt_BR
dc.contributor.affiliationNational Research Council (CNR), Section of Padova, Neuroscience Institutept_BR
dc.description.unidadeInstituto de Ciências Biológicas (IB)pt_BR
dc.description.unidadeDepartamento de Genética e Morfologia (IB GEM)pt_BR
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