ArticleCardiovascular research2014
Reversible and irreversible differentiation of cardiac fibroblasts.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 95 citations in OpenAlex.
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- The Degeneration Paradox: Severely Degenerated Cervical Nucleus Pulposus Cells Display Enhanced Mechanoplasticity Under Moderate Cyclic Tensile Strain.Biomolecules · 2026Article
- Myogenic Differentiation (MyoD) Gene Expression in Cornea and Role in Corneal Myofibroblast Dedifferentiation.Investigative ophthalmology & visual science · 2026Article
- Simultaneous induction of differentiation and senescence in cardiac fibroblasts by TGF-β1: effects of senotherapeutics drugs.Frontiers in pharmacology · 2026Article
- Uridine-Cytidine Kinase 2 (UCK2)/Uridine-Cytidine Kinase Like 1 (UCKL1) complex exacerbates the differentiation of myocardial fibroblasts via TRIM21/Smurf2/Smad3 pathway after myocardial infarction.Molecular biomedicine · 2025Article
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- HSPA12A acts as a scaffolding protein to inhibit cardiac fibroblast activation and cardiac fibrosis.Journal of advanced research · 2025Article
- Cardiac fibroblasts: answering the call.American journal of physiology. Heart and circulatory physiology · 2024Review
- Opto-SICM framework combines optogenetics with scanning ion conductance microscopy for probing cell-to-cell contacts.Communications biology · 2023Article
- Exploring the relationship between epigenetic DNA methylation and cardiac fibrosis through Raman microspectroscopy.American journal of physiology. Cell physiology · 2023Article
- Reduction, proliferation, and differentiation defects of stem cells over time: a consequence of selective accumulation of old centrioles in the stem cells?Molecular biology reports · 2023Review
- Endothelin-1 Induces Cell Proliferation and Myofibroblast Differentiation through the ETInternational journal of molecular sciences · 2023Article
- Circ-sh3rf3/GATA-4/miR-29a regulatory axis in fibroblast-myofibroblast differentiation and myocardial fibrosis.Cellular and molecular life sciences : CMLS · 2023Article
- A positive mechanobiological feedback loop controls bistable switching of cardiac fibroblast phenotype.Cell discovery · 2022Article
- MicroRNA-130a attenuates cardiac fibrosis after myocardial infarction through TGF-β/Smad signaling by directly targeting TGF-β receptor 1.Bioengineered · 2022Article
- Transcriptome and proteome profiling of activated cardiac fibroblasts supports target prioritization in cardiac fibrosis.Frontiers in cardiovascular medicine · 2022Article
- Dexmedetomidine Promotes Lipopolysaccharide-Induced Differentiation of Cardiac Fibroblasts and Collagen I/III Synthesis through αInternational journal of molecular sciences · 2021Article
- A deep learning approach to identify and segment alpha-smooth muscle actin stress fiber positive cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsDifferentiation of cardiac fibroblasts (Fbs) into myofibroblasts (MyoFbs) is responsible for connective tissue build-up in myocardial remodelling. We examined MyoFb differentiation and reversibility. METHODS AND
resultsAdult rat cardiac Fbs were cultured on a plastic substratum providing mechanical stress, with conditions to obtain different levels of Fb differentiation. Fb spontaneously differentiated to proliferating MyoFb (p-MyoFb) with stress fibre formation decorated with alpha-smooth muscle actin (α-SMA). Transforming growth factor-β1 (TGF-β1) promoted differentiation into α-SMA-positive MyoFb showing near the absence of proliferation, i.e. non-p-MyoFb. SD-208, a TGF-β-receptor-I (TGF-β-RI) kinase blocker, inhibited p-MyoFb differentiation as shown by stress fibre absence, low α-SMA expression, and high proliferation levels. Fb seeded in collagen matrices induced no contraction, whereas p-MyoFb and non-p-MyoFb induced 2.5- and four-fold contraction. Fb produced little collagen but high levels of interleukin-10. Non-p-MyoFb had high collagen production and high monocyte chemoattractant protein-1 and tissue inhibitor of metalloproteinases-1 levels. Transcriptome analysis indicated differential activation of gene networks related to differentiation of MyoFb (e.g. paxilin and PAK) and reduced proliferation of non-p-MyoFb (e.g. cyclins and cell cycle regulation). Dedifferentiation of p-MyoFb with stress fibre de-polymerization, but not of non-p-MyoFb, was induced by SD-208 despite maintained stress. Stress fibre de-polymerization could also be induced by mechanical strain release in p-MyoFb and non-p-MyoFb (2-day cultures in unrestrained 3-D collagen matrices). Only p-MyoFb showed true dedifferentiation after long-term 3-D cultures.
conclusionsFb, p-MyoFb, and non-p-MyoFb have a distinct gene expression, ultrastructural, and functional profile. Both reduction in mechanical strain and TGF-β-RI kinase inhibition can reverse p-MyoFb differentiation but not non-p-MyoFb.
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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.