ReviewPediatric nephrology (Berlin, Germany)2012
The origin of interstitial myofibroblasts in chronic kidney disease.
Review in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 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
115 citing papers in PubMed, 197 citations in OpenAlex.
- Pirfenidone treatment attenuates fibrosis in autosomal dominant polycystic kidney disease.JCI insight · 2026Article
- Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease.Cell communication and signaling : CCS · 2026Article
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).International journal of molecular medicine · 2025Review
- Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025Review
- Intermittent Fasting Protects Against the Progression from Acute Kidney Injury to Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2025Article
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Iguratimod prevents renal fibrosis in unilateral ureteral obstruction model mice by suppressing M2 macrophage infiltration and macrophage-myofibroblast transition.Renal failure · 2024Article
- Alantolactone alleviates epithelial-mesenchymal transition by regulating the TGF-β/STAT3 signaling pathway in renal fibrosis.Heliyon · 2024Article
- Stem cell-based therapy for fibrotic diseases: mechanisms and pathways.Stem cell research & therapy · 2024Review
- From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Alantolactone Attenuates Renal Fibrosis via Inhibition of Transforming Growth Factor β/Smad3 Signaling Pathway.Diabetes & metabolism journal · 2024Article
- Circ_0001666 upregulation promotes intestinal epithelial cell fibrosis in pediatric Crohn's disease via the SRSF1/BMP7 axis.The Kaohsiung journal of medical sciences · 2023Article
- FUT1-mediated terminal fucosylation acts as a new target to attenuate renal fibrosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Lung fibrosis: Post-COVID-19 complications and evidences.International immunopharmacology · 2023Review
- Low nephron endowment increases susceptibility to renal stress and chronic kidney disease.JCI insight · 2023Article
- Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Urine-Derived Stem Cell-Secreted Klotho Plays a Crucial Role in the HK-2 Fibrosis Model by Inhibiting the TGF-β Signaling Pathway.International journal of molecular sciences · 2022Article
55 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
3 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic kidney diseases (CKD), independent of their primary cause, lead to progressive, irreversible loss of functional renal parenchyma. Renal pathology in CKD is characterized by tubulointerstitial fibrosis with excessive matrix deposition produced by myofibroblasts. Because blocking the formation of these scar-forming cells represents a logical therapeutic target for patients with progressive fibrotic kidney disease, the origin of renal myofibroblasts is a subject of intense investigation. Although the traditional view holds that resident fibroblasts are the myofibroblast precursor, for the last 10 years, injured epithelial cells have been thought to directly contribute to the myofibroblast pool by the process of epithelial-to-mesenchymal transition (EMT). The recent application of genetic fate mapping techniques in mouse fibrosis models has provided new insights into the cell hierarchies in fibrotic kidney disease and results cast doubt on the concept that EMT is a source of myofibroblast recruitment in vivo, but rather point to the resident pericyte/perivascular fibroblast as the myofibroblast progenitor pool. This review will highlight recent findings arguing against EMT as a direct contributor to the kidney myofibroblast population and review the use of genetic fate mapping to elucidate the cellular mechanisms of kidney homeostasis and disease.
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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.