Therapeutic potential of oleic acid supplementation in myotonic dystrophy muscle cell models.
Nerea MorenoMaria Sabater-ArcisTeresa SevillaManuel Perez AlonsoJessica OhanaAriadna BargielaRuben ArteroPublished in: Biological research (2024)
For the first time in DM1, we describe a fatty acid metabolism impairment that originated, at least in part, from a decrease in SCD1. Because OA allosterically inhibits MSI2 binding to molecular targets, reduced OA levels synergize with the overexpression of MSI2 and contribute to the MSI2 > miR-7 > autophagy axis that we proposed to explain the muscle atrophy phenotype.
Keyphrases
- cell proliferation
- fatty acid
- skeletal muscle
- knee osteoarthritis
- long non coding rna
- single cell
- cell death
- endoplasmic reticulum stress
- cell therapy
- signaling pathway
- early onset
- oxidative stress
- transcription factor
- stem cells
- type diabetes
- glycemic control
- mesenchymal stem cells
- single molecule
- muscular dystrophy