ArticleScientific reports2018
Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment.Stem cell research & therapy · 2026Article
- Gene therapy CM-YAPNature cardiovascular research · 2025Article
- Role of tumor microenvironment in ovarian cancer metastasis and clinical advancements.Journal of translational medicine · 2025Review
- Mitochondria‑derived peptides: Promising microproteins in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Intrapericardial injection of hydrogels with ASC and their secretome to treat dilated cardiomyopathies.Scientific reports · 2025Article
- Inhibition and reversal of a TGF-β1 induced myofibroblast phenotype by adipose tissue-derived paracrine factors.Stem cell research & therapy · 2024Article
- Impaired Relaxation in Induced Pluripotent Stem Cell-Derived Cardiomyocytes with PathogenicJournal of the American Heart Association · 2024Article
- Effects of Blood-Derived Products on Cellular Senescence and Inflammatory Response: A Study on Skin Rejuvenation.Current issues in molecular biology · 2024Article
- Pathogenic Roles of Cardiac Fibroblasts in Pediatric Dilated Cardiomyopathy.Journal of the American Heart Association · 2023Article
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- Transcriptome analysis of a dog model of congestive heart failure shows that collagen-related 2-oxoglutarate-dependent dioxygenases contribute to heart failure.Scientific reports · 2022Article
- Role of Mesenchymal Stem Cells and Extracellular Vesicles in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2022Review
- Functions of exogenous FGF signals in regulation of fibroblast to myofibroblast differentiation and extracellular matrix protein expression.Open biology · 2022Review
- Adipose-derived stromal cells increase the formation of collagens through paracrine and juxtacrine mechanisms in a fibroblast co-culture model utilizing macromolecular crowding.Stem cell research & therapy · 2022Article
- Anti-fibrotic effects of pharmacologic FGF-2: a review of recent literature.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Review
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- The Role of Mitochondria-Derived Peptides in Cardiovascular Diseases and Their Potential as Therapeutic Targets.International journal of molecular sciences · 2021Review
- Stromal Heterogeneity in the Human Proliferative Endometrium-A Single-Cell RNA Sequencing Study.Journal of personalized medicine · 2021Article
- Engineered macrophage membrane-enveloped nanomedicine for ameliorating myocardial infarction in a mouse model.Bioengineering & translational medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which can antagonize TGF-β1 signaling. We hypothesized that TGF-β1-induced cardiac fibroblast to myofibroblast differentiation is abrogated by FGF-2 and ASC conditioned medium (ASC-CMed). Our experiments demonstrated that TGF-β1 treatment-induced cardiac fibroblast differentiation into myofibroblasts, as evidenced by the formation of contractile stress fibers rich in αSMA. FGF-2 blocked the differentiation, as evidenced by the reduction in gene (TAGLN, p < 0.0001; ACTA2, p = 0.0056) and protein (αSMA, p = 0.0338) expression of mesenchymal markers and extracellular matrix components gene expression (COL1A1, p < 0.0001; COL3A1, p = 0.0029). ASC-CMed did not block myofibroblast differentiation. The treatment with FGF-2 increased matrix metalloproteinases gene expression (MMP1, p < 0.0001; MMP14, p = 0.0027) and decreased the expression of tissue inhibitor of metalloproteinase gene TIMP2 (p = 0.0023). ASC-CMed did not influence these genes. The proliferation of TGF-β1-induced human cardiac fibroblasts was restored by both FGF-2 (p = 0.0002) and ASC-CMed (p = 0.0121). The present study supports the anti-fibrotic effects of FGF-2 through the blockage of cardiac fibroblast differentiation into myofibroblasts. ASC-CMed, however, did not replicate the anti-fibrotic effects of FGF-2 in vitro.
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