MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
Open accessAbstract
Thioredoxin reductase 1 (TrxR1) is a selenocysteine-containing protein involved in cellular redox homeostasis which is downregulated in skeletal muscle differentiation. Here we show that TrxR1 decrease occurring during myogenesis is functionally involved in the coordination of this cellular process. Indeed, TrxR1 depletion reduces myoblasts growth by inducing an early myogenesis -related gene expression pattern which includes myogenin and Myf5 up-regulation and Cyclin D1 decrease. On the contrary, the overexpression of TrxR1 during differentiation delays myogenic process, by negatively affecting the expression of Myogenin and MyHC. Moreover, we found that miR-23a and miR-23b - whose expression was increased in the early stage of C2C12 differentiation - are involved in the regulation of TrxR1 expression through their direct binding to the 3′ UTR of TrxR1 mRNA. Interestingly, the forced inhibition of miR-23a and miR-23b during C2C12 differentiation partially rescues TrxR1 levels and delays the expression of myogenic markers, suggesting the involvement of miR-23 in myogenesis via TrxR1 repression. Taken together, our results depict for the first time a novel molecular axis, which functionally acts in skeletal muscle differentiation through the modulation of TrxR1 by miR-23.
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miR-23a and miR-23b share a common target and have consistent functions, affecting skeletal muscle differentiation by inhibiting TrxR1 and participating in skeletal muscle generation.
“miR-23a and miR-23b share a common target and have consistent functions, which can affect skeletal muscle differentiation by inhibiting Thioredoxin reductase 1 (TrxR1) and participate in skeletal muscle generation [[104], [105], [106]].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [106]
In horse cell reprogramming, miR-23 expression level was decreased in induced pluripotent stem cells, which can recognize breed characteristics of horses.
“the expression level of miR-23 was decreased in induced pluripotent stem cells (iPSCs), which can recognize the breed characteristics of horses.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [106]
The Results describe miR-23 experiments in C2C12 mouse myoblasts, and the Methods describe mouse muscle cells; no page numbers are provided in our copy. Searches for horse cell reprogramming, induced pluripotent stem cells, and breed characteristics found no passage addressing a decrease in miR-23 in horse iPSCs or their ability to identify breeds. (LLM, conf=0.76)
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Epigenomic adaptations of exercise in the control of metabolic disease and cancer
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CircHOMER1 in mediating porcine skeletal muscle development
Li, M., Gong, Y., Ma, S., Chen, J., Zhang, W., Yang, Y., Cao, G., Guo, X., & Li, B. (2025) · BMC Genomics · doi:10.1186/s12864-025-11991-2
Selenium in aging and longevity
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- Authors
- Mercatelli, N., Fittipaldi, S., De Paola, E., Dimauro, I., Paronetto, M. P., Jackson, M. J., & Caporossi, D.
- Affiliations
- Foro Italico University of Rome (IT)
- University of Liverpool (GB)
- Corresponding author
- Mercatelli, Neri
- ORCID
- Venue
- Scientific Reports
- Published
- 2017-08-03
- Volume
- 7
- Issue
- 1
- Pages
- 7219-7219
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5543121
- OpenAlex
- W2739709130
- Cited by
- 49
- References
- 48
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 3 · 2022: 3 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 5 · 2017: 2
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca (PRIN2012)
- Medical Research Council (MR/K006312/1, MR/P020941/1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- miR-23a, miR-23b, thioredoxin reductase 1, skeletal muscle differentiation, myogenesis, microRNA regulation, 3' untranslated region, myogenin, Myf5, cyclin D1, myosin heavy chain, C2C12 myoblasts, redox homeostasis, selenocysteine
- MeSH terms
- Ectopic Gene Expression, Animals, Binding Sites, Cell Differentiation, Cell Line, Gene Expression Regulation, Biomarkers, Genes, Reporter, Muscle, Skeletal, 3' Untranslated Regions, Muscle Development, Myoblasts, RNA Interference, MicroRNAs, Mice, Thioredoxin Reductase 1
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