ArticleNature medicine2013
Origin and function of myofibroblasts in kidney fibrosis.
Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 751 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.
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Who cites it
751 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,221 citations in OpenAlex.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- Activation of the TGF-β1/HIPK2 signaling pathway exacerbates EMT injury in renal tubular epithelial cells in diabetic kidney disease.Renal failure · 2026Article
- Unmasking Early Hepatorenal Fibrosis in Polycystic Kidney Disease Using Noninvasive Precision Molecular MRI of Collagen.bioRxiv : the preprint server for biology · 2026Article
- Renal Tubular Epithelial Cells Senescence Induced by 1-Aminopyrene Activates Fibroblast via BRD4 Driven Senescence-Associated Secretory Phenotype Signaling.Journal of biochemical and molecular toxicology · 2026Article
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- TNFα and endothelial IL-1 receptor signaling drive peritubular capillary regression and mature collagen accumulation in obstructive kidney injury.American journal of physiology. Renal physiology · 2026Article
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Pirfenidone treatment attenuates fibrosis in autosomal dominant polycystic kidney disease.JCI insight · 2026Article
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026Review
- Pericyte-myofibroblast transition: a novel mechanism in peritoneal fibrosis and the effect of Asiaticoside.Journal of advanced research · 2026Article
- Kidney Elastography in Adult Nephrology: A Narrative Review.Diagnostics (Basel, Switzerland) · 2026Review
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- Piezo1 promote macrophage-to-myofibroblast transition and bladder fibrosis in neurogenic bladder.World journal of urology · 2026Article
- Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease.Cell communication and signaling : CCS · 2026Article
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- Low-intensity extracorporeal shock wave therapy ameliorates fibrosis and renal function in a preclinical model of chronic kidney disease.Anatomy & cell biology · 2026Article
- Review
- Research Progress on the Treatment of Renal Injury with Esculetin: Multi-Target Pharmacological Mechanism and Clinical Translation Prospect.International journal of molecular sciences · 2026Review
691 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Myofibroblasts are associated with organ fibrosis, but their precise origin and functional role remain unknown. We used multiple genetically engineered mice to track, fate map and ablate cells to determine the source and function of myofibroblasts in kidney fibrosis. Through this comprehensive analysis, we identified that the total pool of myofibroblasts is split, with 50% arising from local resident fibroblasts through proliferation. The nonproliferating myofibroblasts derive through differentiation from bone marrow (35%), the endothelial-to-mesenchymal transition program (10%) and the epithelial-to-mesenchymal transition program (5%). Specific deletion of Tgfbr2 in α-smooth muscle actin (αSMA)(+) cells revealed the importance of this pathway in the recruitment of myofibroblasts through differentiation. Using genetic mouse models and a fate-mapping strategy, we determined that vascular pericytes probably do not contribute to the emergence of myofibroblasts or fibrosis. Our data suggest that targeting diverse pathways is required to substantially inhibit the composite accumulation of myofibroblasts in kidney fibrosis.
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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.