ReviewNature reviews. Nephrology2015
Diverse origins of the myofibroblast—implications for kidney fibrosis.
Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- Potential association between elevated serum human epididymis protein 4 and renal fibrosis: A systemic review and meta-analysis.Medicine · 2017Pooled it
- Pericyte-myofibroblast transition: a novel mechanism in peritoneal fibrosis and the effect of Asiaticoside.Journal of advanced research · 2026Article
- Matrix Gla Protein is a novel regulator of TGFβ-dependent fibroblast activation and kidney fibrosis.Molecular biomedicine · 2026Article
- Peroxidasin expression patterns predict fibrosis and kidney function decline in IgA nephropathy.Clinical and experimental nephrology · 2026Article
- Article
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- The roles of free-fatty acid receptors in the pathophysiology of renal disorders.The Journal of pharmacology and experimental therapeutics · 2026Review
- Inhibition of (interstitial) P2YResearch square · 2026Article
- Chrysogenones A-E: Malonyl-Modified Ergosterone Derivatives from Deep-Sea-DerivedMarine drugs · 2026Article
- Matrix Gla Protein Expression in Pericytes and Myofibroblasts Contributes to Renal Fibrosis.The American journal of pathology · 2026Article
- Inhibition of (interstitial) P2YbioRxiv : the preprint server for biology · 2026Article
- Sema3dInternational journal of biological sciences · 2026Article
- Overexpression of Thrombomodulin in Adipose-Derived Mesenchymal Stem Cells Reduces Thrombogenic Risk and Enhances Therapeutic Efficacy.Journal of the American Society of Nephrology : JASN · 2026Article
- Epigenetic Suppression of RASAL1 by HDAC3 and Cofactor YY1 Promotes Fibroblast-Myofibroblast Transition and Renal Fibrosis.Research (Washington, D.C.) · 2026Article
- Tracing the origin of myofibroblasts in kidney fibrosis.Nature communications · 2025Article
- The novel circular RNA circG6pc attenuates oxidative stress and mitochondrial damage through miR-7018-5p/Aldh6a1 axis in kidney fibrosis.Cellular & molecular biology letters · 2025Article
- Comprehensive analysis of pyroptosis-related gene signatures in renal fibrosis.Clinical and experimental nephrology · 2025Article
- Progress of functional magnetic resonance imaging in the assessment of transplanted kidney function.Renal failure · 2025Review
- Exosomal miR-122-5p from tubular cells ameliorates renal interstitial fibrosis by regulating fibroblasts via HIF-1α.Cell death discovery · 2025Article
115 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
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is the common end point of chronic kidney disease. The persistent production of inflammatory cytokines and growth factors leads to an ongoing process of extracellular matrix production that eventually disrupts the normal functioning of the organ. During fibrosis, the myofibroblast is commonly regarded as the predominant effector cell. Accumulating evidence has demonstrated a diverse origin of myofibroblasts in kidney fibrosis. Proposed major contributors of myofibroblasts include bone marrow-derived fibroblasts, tubular epithelial cells, endothelial cells, pericytes and interstitial fibroblasts; the published data, however, have not yet clearly defined the relative contribution of these different cellular sources. Myofibroblasts have been reported to originate from various sources, irrespective of the nature of the initial damage responsible for the induction of kidney fibrosis. Here, we review the possible relevance of the diversity of myofibroblast progenitors in kidney fibrosis and the implications for the development of novel therapeutic approaches. Specifically, we discuss the current status of preclinical and clinical antifibrotic therapy and describe targeting strategies that might help support resident and circulating cells to maintain or regain their original functional differentiation state. Such strategies might help these cells resist their transition to a myofibroblast phenotype to prevent, or even reverse, the fibrotic state.
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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.