Página principal > Artículos > Differentially expressed lncRNAs in SOD1G93A mice skeletal muscle: H19, Myhas and Neat1 as potential biomarkers in amyotrophic later
Resumen: Amyotrophic lateral sclerosis (ALS) is a devastating neuromuscular disease characterized by progressive motor function and muscle mass loss. Despite extensive research in the field, the underlying causes of ALS remain incompletely understood, contributing to the absence of specific diagnostic and prognostic biomarkers and effective therapies. This study investigates the expression of long-non-coding RNAs (lncRNAs) in skeletal muscle as a potential source of biomarkers and therapeutic targets for the disease. The expression profiles of 12 lncRNAs, selected from the literature, were evaluated across different disease stages in tissue and muscle biopsies from the SOD1G93A transgenic mouse model of ALS. Nine out of the 12 lncRNAs were differentially expressed, with Pvt1, H19 and Neat1 showing notable increases in the symptomatic stages of the disease, and suggesting their potential as candidate biomarkers to support diagnosis and key players in muscle pathophysiology in ALS. Furthermore, the progression of Myhas and H19 RNA levels across disease stages correlated with longevity in the SOD1G93A animal model, effectively discriminating between long- and short-term survival individuals, thereby highlighting their potential as prognostic indicators. These findings underscore the involvement of lncRNAs, especially H19 and Myhas, in ALS pathophysiology, offering novel insights for diagnostic, prognostic and therapeutic targets. Idioma: Inglés DOI: 10.1098/rsob.240015 Año: 2024 Publicado en: Open biology 14, 10 (2024), 10 pp. ISSN: 2046-2441 Financiación: info:eu-repo/grantAgreement/ES/DGA/A19-23R Financiación: info:eu-repo/grantAgreement/ES/FIS/PI21-00286 Financiación: info:eu-repo/grantAgreement/ES/ISCIII/CB18-05-0037 Financiación: info:eu-repo/grantAgreement/ES/ISCIII/FEDER/PI21-00372 Financiación: info:eu-repo/grantAgreement/ES/MCIU/FPU19-05625 Financiación: info:eu-repo/grantAgreement/ES/MICINN-AEI/PRTR-C17.I1 Tipo y forma: Artículo (Versión definitiva) Área (Departamento): Área Genética (Dpto. Anatom.,Embri.Genét.Ani.) Área (Departamento): Área Farmacología (Dpto. Farmac.Fisiol.y Med.L.F.)