ArticleNature communications2015
MBNL1-mediated regulation of differentiation RNAs promotes myofibroblast transformation and the fibrotic response.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
69 citing papers in PubMed, 91 citations in OpenAlex.
- Cardiac fibroblast deletion of PTBP1 modulates the profibrotic response by alternative splicing.Nature communications · 2026Article
- Article
- Seta-Inspired Mechano-Intelligent Janus Bandage with Coordinated Adhesion-Contraction for Minimizing Scarring.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- MBNL1 Promotes Intestinal Fibrosis via RAS-MAPK Pathway-Mediated Fibroblast Activation and Proliferation.Biomedicines · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Review
- MBNL proteins in health, disease, and therapeutic applications.Nucleic acids research · 2026Review
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- Promoter-targeted small RNA duplexes increase MBNL1 transcription and mitigate myotonic dystrophy-associated spliceopathy.Nucleic acids research · 2025Article
- Article
- Biological function of RNA-binding proteins in myocardial infarction: a potential emerging therapeutic limelight.Cell & bioscience · 2025Review
- Regulatory roles of PIWI-interacting RNAs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2025Review
- Functions of the Muscleblind-like protein family and their role in disease.Cell communication and signaling : CCS · 2025Review
- Best evidence linking the extracellular factor TGF-β to cancer-associated alternative splicing programs.BBA advances · 2025Review
- Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals.Animal models and experimental medicine · 2025Review
- MBNL1 Regulates Programmed Postnatal Switching Between Regenerative and Differentiated Cardiac States.Circulation · 2024Article
- RNA-binding proteins in cardiovascular biology and disease: the beat goes on.Nature reviews. Cardiology · 2024Review
- In Vitro Assessment of Cardiac Fibroblast Activation at Physiologic Stiffness.Current protocols · 2024Article
- RNA binding proteins as mediators of pathological cardiac remodeling.Frontiers in cell and developmental biology · 2024Review
- Skin treatment with non-thermal plasma modulates the immune system through miR-223-3p and its target genes.RNA biology · 2024Article
9 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
8 authors at 4 institutions in 1 country.
Funding
Abstract
The differentiation of fibroblasts into myofibroblasts mediates tissue wound healing and fibrotic remodelling, although the molecular programme underlying this process remains poorly understood. Here we perform a genome-wide screen for genes that control myofibroblast transformation, and identify the RNA-binding protein muscleblind-like1 (MBNL1). MBNL1 overexpression promotes transformation of fibroblasts into myofibroblasts, whereas loss of Mbnl1 abrogates transformation and impairs the fibrotic phase of wound healing in mouse models of myocardial infarction and dermal injury. Mechanistically, MBNL1 directly binds to and regulates a network of differentiation-specific and cytoskeletal/matrix-assembly transcripts to promote myofibroblast differentiation. One of these transcripts is the nodal transcriptional regulator serum response factor (SRF), whereas another is calcineurin Aβ. CRISPR-Cas9-mediated gene-editing of the MBNL1-binding site within the Srf 3'UTR impairs myofibroblast differentiation, whereas in vivo deletion of Srf in fibroblasts impairs wound healing and fibrosis. These data establish a new RNA-dependent paradigm for myofibroblast formation through MBNL1.
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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.