ArticleThe Journal of clinical investigation2011
Mice lacking microRNA 133a develop dynamin 2–dependent centronuclear myopathy.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
99 citing papers in PubMed, 157 citations in OpenAlex.
- DNM2 lipid binding drives centronuclear myopathy and represents a potential therapeutic target.JCI insight · 2026Article
- Muscle-Specific DNM2 Overexpression Improves Charcot-Marie-Tooth Disease In Vivo and Reveals a Narrow Therapeutic Window in Skeletal Muscle.International journal of molecular sciences · 2026Article
- Exon skipping peptide-conjugated morpholinos downregulate dynamin 2 to rescue centronuclear myopathy.Brain : a journal of neurology · 2025Article
- Article
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- microRNA-133a as an indicator of disease progression and treatment response in X-linked myotubular myopathy.Molecular therapy. Nucleic acids · 2025Article
- Combining dynamin 2 myopathy and neuropathy mutations rescues both phenotypes.Nature communications · 2025Article
- Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).Biomedical reports · 2025Review
- Potential compensatory mechanisms preserving cardiac function in myotubular myopathy.Cellular and molecular life sciences : CMLS · 2024Article
- DNM2 levels normalization improves muscle phenotypes of a novel mouse model for moderate centronuclear myopathy.Molecular therapy. Nucleic acids · 2023Article
- Regulation of muscle stem cell fate.Cell regeneration (London, England) · 2022Review
- The link between gestational diabetes and cardiovascular diseases: potential role of extracellular vesicles.Cardiovascular diabetology · 2022Review
- Postnatal Protein Intake as a Determinant of Skeletal Muscle Structure and Function in Mice-A Pilot Study.International journal of molecular sciences · 2022Article
- Biomarkers of Frailty: miRNAs as Common Signatures of Impairment in Cognitive and Physical Domains.Biology · 2022Review
- Ribonucleotide reductase M2B in the myofibers modulates stem cell fate in skeletal muscle.NPJ Regenerative medicine · 2022Article
- Natural history of a mouse model of X-linked myotubular myopathy.Disease models & mechanisms · 2022Article
- Natural history study and statistical modeling of disease progression in a preclinical model of myotubular myopathy.Disease models & mechanisms · 2022Article
- Characterization of a novel zebrafish model of SPEG-related centronuclear myopathy.Disease models & mechanisms · 2022Article
- Benefits of therapy by dynamin-2-mutant-specific silencing are maintained with time in a mouse model of dominant centronuclear myopathy.Molecular therapy. Nucleic acids · 2022Article
- BIN1 modulation in vivo rescues dynamin-related myopathy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
MicroRNAs modulate cellular phenotypes by inhibiting expression of mRNA targets. In this study, we have shown that the muscle-specific microRNAs miR-133a-1 and miR-133a-2 are essential for multiple facets of skeletal muscle function and homeostasis in mice. Mice with genetic deletions of miR-133a-1 and miR-133a-2 developed adult-onset centronuclear myopathy in type II (fast-twitch) myofibers, accompanied by impaired mitochondrial function, fast-to-slow myofiber conversion, and disarray of muscle triads (sites of excitation- contraction coupling). These abnormalities mimicked human centronuclear myopathies and could be ascribed, at least in part, to dysregulation of the miR-133a target mRNA that encodes dynamin 2, a GTPase implicated in human centronuclear myopathy. Our findings reveal an essential role for miR-133a in the maintenance of adult skeletal muscle structure, function, bioenergetics, and myofiber identity; they also identify a potential modulator of centronuclear myopathies.
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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.