ArticlePloS one2012
Hmgb3 is regulated by microRNA-206 during muscle regeneration.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- A positively selected microRNA controls a reversible aging program in striated muscle.bioRxiv : the preprint server for biology · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Hormesis and Muscle Plasticity.Advances in experimental medicine and biology · 2025Review
- Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024Review
- miRNome Profiling Detects miR-101-3p and miR-142-5p as Putative Blood Biomarkers of Frailty Syndrome.Genes · 2022Article
- The roles of microRNA in redox metabolism and exercise-mediated adaptation.Journal of sport and health science · 2020Review
- Muscle miRNAome shows suppression of chronic inflammatory miRNAs with both prednisone and vamorolone.Physiological genomics · 2018Article
- Non-coding RNAs in muscle differentiation and musculoskeletal disease.The Journal of clinical investigation · 2016Review
- Translating golden retriever muscular dystrophy microarray findings to novel biomarkers for cardiac/skeletal muscle function in Duchenne muscular dystrophy.Pediatric research · 2016Article
- Stem cell activation in skeletal muscle regeneration.Cellular and molecular life sciences : CMLS · 2015Review
- MicroRNA-206 regulates surfactant secretion by targeting VAMP-2.FEBS letters · 2015Article
- Article
- The role of microRNAs in skeletal muscle health and disease.Frontiers in bioscience (Landmark edition) · 2015Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Upregulation of miR-513b inhibits cell proliferation, migration, and promotes apoptosis by targeting high mobility group-box 3 protein in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- MicroRNA-206 overexpression promotes apoptosis, induces cell cycle arrest and inhibits the migration of human hepatocellular carcinoma HepG2 cells.International journal of molecular medicine · 2014Article
- Thermal plasticity of the miRNA transcriptome during Senegalese sole development.BMC genomics · 2014Article
- ADAR1 deaminase contributes to scheduled skeletal myogenesis progression via stage-specific functions.Cell death and differentiation · 2014Article
- Converging pathways involving microRNA-206 and the RNA-binding protein KSRP control post-transcriptionally utrophin A expression in skeletal muscle.Nucleic acids research · 2014Article
- MicroRNA-206: a potential circulating biomarker candidate for amyotrophic lateral sclerosis.PloS one · 2014Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundMicroRNAs (miRNAs) have been recently involved in most of human diseases as targets for potential strategies to rescue the pathological phenotype. Since the skeletal muscle is a spread-wide highly differentiated and organized tissue, rescue of severely compromised muscle still remains distant from nowadays. For this reason, we aimed to identify a subset of miRNAs major involved in muscle remodelling and regeneration by analysing the miRNA-profile of single fibres isolated from dystrophic muscle, which was here considered as a model of chronic damage. METHODOLOGY/PRINCIPAL
findingsThe miRNA-signature associated to regenerating (newly formed) and remodelling (resting) fibres was investigated in animal models of muscular dystrophies and acute damage, in order to distinguish which miRNAs are primary related to muscle regeneration. In this study we identify fourteen miRNAs associated to dystrophic fibres responsible for muscle regeneration and remodelling, and confirm over-expression of the previously identified regeneration-associated myomiR-206. In particular, a functional binding site for myomiR-206 was identified and validated in the 3'untranslated region (3'UTR) of an X-linked member of a family of sequence independent chromatin-binding proteins (Hmgb3) that is preferentially expressed in hematopoietic stem cells. During regeneration of single muscle fibres, Hmgb3 messenger RNA (mRNA) and protein expression was gradually reduced, concurrent with the up-regulation of miR-206. CONCLUSION/SIGNIFICANCE: Our results elucidate a negative feedback circuit in which myomiR-206 represses Hmgb3 expression to modulate the regeneration of single muscle fibres after acute and chronic muscle damage. These findings suggest that myomiR-206 may be a potential therapeutic target in muscle diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.