ArticleJournal of cachexia, sarcopenia and muscle2021
H19X-encoded miR-322(424)/miR-503 regulates muscle mass by targeting translation initiation factors.
Article in Journal of cachexia, sarcopenia and muscle, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Metrics of left ventricular active relaxation reflect proteomic myocardial remodelling and reverse remodelling.ESC heart failure · 2026Article
- Article
- Endocrine-exocrine miR-503-322 drives aging-associated pancreatitis via targeting MKNK1 in acinar cells.Nature communications · 2025Article
- Methylome-proteome integration after late-life voluntary exercise training reveals regulation and target information for improved skeletal muscle health.The Journal of physiology · 2025Article
- Network-based modelling reveals cell-type enriched patterns of non-coding RNA regulation during human skeletal muscle remodelling.bioRxiv : the preprint server for biology · 2024Article
- Network-based modelling reveals cell-type enriched patterns of non-coding RNA regulation during human skeletal muscle remodelling.NAR molecular medicine · 2024Article
- Review
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Identification of Unique microRNA Profiles in Different Types of Idiopathic Inflammatory Myopathy.Cells · 2023Article
- eIF2Bδ blocks the integrated stress response and maintains eIF2B activity and cancer metastasis by overexpression in breast cancer stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles.Biomolecules · 2022Article
- H19X-encoded miR-322(424)/miR-503 regulates muscle mass by targeting translation initiation factors.Journal of cachexia, sarcopenia and muscle · 2021Article
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Authors and funding
20 authors at 5 institutions in 2 countries.
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Abstract
backgroundSkeletal muscle atrophy is a debilitating complication of many chronic diseases, disuse conditions, and ageing. Genome-wide gene expression analyses have identified that elevated levels of microRNAs encoded by the H19X locus are among the most significant changes in skeletal muscles in a wide scope of human cachectic conditions. We have previously reported that the H19X locus is important for the establishment of striated muscle fate during embryogenesis. However, the role of H19X-encoded microRNAs in regulating skeletal mass in adults is unknown.
methodsWe have created a transgenic mouse strain in which ectopic expression of miR-322/miR-503 is driven by the skeletal muscle-specific muscle creatine kinase promoter. We also used an H19X mutant mouse strain in which transcription from the locus is interrupted by a gene trap. Animal phenotypes were analysed by standard histological methods. Underlying mechanisms were explored by using transcriptome profiling and validated in the two animal models and cultured myotubes.
resultsOur results demonstrate that the levels of H19X microRNAs are inversely related to postnatal skeletal muscle growth. Targeted overexpression of miR-322/miR-503 impeded skeletal muscle growth. The weight of gastrocnemius muscles of transgenic mice was only 54.5% of the counterparts of wild-type littermates. By contrast, interruption of transcription from the H19X locus stimulates postnatal muscle growth by 14.4-14.9% and attenuates the loss of skeletal muscle mass in response to starvation by 12.8-21.0%. Impeded muscle growth was not caused by impaired IGF1/AKT/mTOR signalling or a hyperactive ubiquitin-proteasome system, instead accompanied by markedly dropped abundance of translation initiation factors in transgenic mice. miR-322/miR-503 directly targets eIF4E, eIF4G1, eIF4B, eIF2B5, and eIF3M.
conclusionsOur study illustrates a novel pathway wherein H19X microRNAs regulate skeletal muscle growth and atrophy through regulating the abundance of translation initiation factors, thereby protein synthesis. The study highlights how translation initiation factors lie at the crux of multiple signalling pathways that control skeletal muscle mass.
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