ArticleActa physiologica (Oxford, England)2019
miR-29c improves skeletal muscle mass and function throughout myocyte proliferation and differentiation and by repressing atrophy-related genes.
Article in Acta physiologica (Oxford, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Skeletal Muscle MicroRNA Patterns in Response to a Single Bout of Exercise in Females: Biomarkers for Subsequent Training Adaptation?Biomolecules · 2023Trial
- A circRNA-miRNA-mRNA network potentially regulates skeletal muscle adaptation to hypoxia in Tibetan sheep.BMC genomics · 2026Article
- The Role of Extracellular Vesicles in Musculoskeletal Diseases.Journal of extracellular vesicles · 2025Review
- Mechanism of exercise-derived circulating exosomes as a target for sarcopenia management.Frontiers in physiology · 2025Review
- Functional Role of Extracellular Vesicles in Skeletal Muscle Physiology and Sarcopenia: The Importance of Physical Exercise and Nutrition.Nutrients · 2024Review
- Identifying microRNAs Possibly Implicated in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia: A Review.International journal of molecular sciences · 2024Review
- HucMSCs Delay Muscle Atrophy After Peripheral Nerve Injury Through Exosomes by Repressing Muscle-Specific Ubiquitin Ligases.Stem cells (Dayton, Ohio) · 2024Article
- Integrated analysis of muscle transcriptome, miRNA, and proteome of Chinese indigenous breed Ningxiang pig in three developmental stages.Frontiers in genetics · 2024Article
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- miR-100-5p Regulates Skeletal Muscle Myogenesis through theInternational journal of molecular sciences · 2023Article
- Small-Molecule Inhibition of MuRF1 Prevents Early Disuse-Induced Diaphragmatic Dysfunction and Atrophy.International journal of molecular sciences · 2023Article
- A pathway analysis-based algorithm for calculating the participation degree of ncRNA in transcriptome.Scientific reports · 2022Article
- miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR.International journal of molecular sciences · 2022Article
- miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles.Biomolecules · 2022Article
- Characterization of the circRNA-miRNA-mRNA Network to Reveal the Potential Functional ceRNAs Associated With Dynamic Changes in the Meat Quality of the Longissimus Thoracis Muscle in Tibetan Sheep at Different Growth Stages.Frontiers in veterinary science · 2022Article
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- Evidence of myomiR regulation of the pentose phosphate pathway during mechanical load-induced hypertrophy.Physiological reports · 2021Article
- Downregulation of miR-29c promotes muscle wasting by modulating the activity of leukemia inhibitory factor in lung cancer cachexia.Cancer cell international · 2021Article
- An Emerging Role for Epigenetics in Cerebral Palsy.Journal of personalized medicine · 2021Review
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
aimTo identify microRNAs (miRs) involved in the regulation of skeletal muscle mass. For that purpose, we have initially utilized an in silico analysis, resulting in the identification of miR-29c as a positive regulator of muscle mass.
methodsmiR-29c was electrotransferred to the tibialis anterior to address its morphometric and functional properties and to determine the level of satellite cell proliferation and differentiation. qPCR was used to investigate the effect of miR-29c overexpression on trophicity-related genes. C2C12 cells were used to determine the impact of miR-29c on myogenesis and a luciferase reporter assay was used to evaluate the ability of miR-29c to bind to the MuRF1 3'UTR.
resultsThe overexpression of miR-29c in the tibialis anterior increased muscle mass by 40%, with a corresponding increase in fibre cross-sectional area and force and a 30% increase in length. In addition, satellite cell proliferation and differentiation were increased. In C2C12 cells, miR-29c oligonucleotides caused increased levels of differentiation, as evidenced by an increase in eMHC immunostaining and the myotube fusion index. Accordingly, the mRNA levels of myogenic markers were also increased. Mechanistically, the overexpression of miR-29c inhibited the expression of the muscle atrophic factors MuRF1, Atrogin-1 and HDAC4. For the key atrogene MuRF1, we found that miR-29c can bind to its 3'UTR to mediate repression.
conclusionsThe results herein suggest that miR-29c can improve skeletal muscle size and function by stimulating satellite cell proliferation and repressing atrophy-related genes. Taken together, our results indicate that miR-29c might be useful as a future therapeutic device in diseases involving decreased skeletal muscle mass.
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