ArticleCurrent pathobiology reports2013
Matrix Producing Cells in Chronic Kidney Disease: Origin, Regulation, and Activation.
Article in Current pathobiology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Preclinical Evaluation of Baicalin for the Treatment of Diabetic Nephropathy: A Systematic Review and Meta-Analysis.Planta medica · 2025Pooled it
- Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2026Article
- Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Perturbed gut microbiota and serum metabolites are associated with progressive renal fibrosis.Frontiers in medicine · 2025Article
- Single-cell sequencing dissects the transcriptional identity of activated fibroblasts and identifies novel persistent distal tubular injury patterns in kidney fibrosis.Scientific reports · 2024Article
- Cep120 is essential for kidney stromal progenitor cell growth and differentiation.EMBO reports · 2024Article
- Review
- High-throughput data on circular RNA reveal novel insights into chronic glomerulonephritis.Genes & genomics · 2023Article
- An update on renal fibrosis: from mechanisms to therapeutic strategies with a focus on extracellular vesicles.Kidney research and clinical practice · 2023Article
- Targeting inflammation for the treatment of Diabetic Kidney Disease: a five-compartment mechanistic model.BMC nephrology · 2022Review
- TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases.Mediterranean journal of rheumatology · 2022Review
- Bone marrow mesenchymal stem cell-derived exosomes improve renal fibrosis by reducing the polarisation of M1 and M2 macrophages through the activation of EP2 receptors.IET nanobiotechnology · 2022Article
- Histone Acetylation and Modifiers in Renal Fibrosis.Frontiers in pharmacology · 2022Review
- The roles of collagen in chronic kidney disease and vascular calcification.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Long Non-coding RNA ENST00000453774.1 Confers an Inhibitory Effect on Renal Fibrosis by Inhibiting miR-324-3p to Promote NRG1 Expression.Frontiers in cell and developmental biology · 2021Article
- The many talents of transforming growth factor-β in the kidney.Current opinion in nephrology and hypertension · 2019Review
- Regulation of Endothelial-to-Mesenchymal Transition by MicroRNAs in Chronic Allograft Dysfunction.Transplantation · 2019Article
- Abnormal expression of fibrosis markers, estrogen receptor α and stromal derived factor‑1/chemokine (C‑X‑C motif) receptor‑4 axis in intrauterine adhesions.International journal of molecular medicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic injury to the kidney causes kidney fibrosis with irreversible loss of functional renal parenchyma and leads to the clinical syndromes of chronic kidney disease (CKD) and end-stage renal disease (ESRD). Regardless of the type of initial injury, kidney disease progression follows the same pathophysiologic processes characterized by interstitial fibrosis, capillary rarefaction and tubular atrophy. Myofibroblasts play a pivotal role in fibrosis by driving excessive extracellular matrix (ECM) deposition. Targeting these cells in order to prevent the progression of CKD is a promising therapeutic strategy, however, the cellular source of these cells is still controversial. In recent years, a growing amount of evidence points to resident mesenchymal cells such as pericytes and perivascular fibroblasts, which form extensive networks around the renal vasculature, as major contributors to the pool of myofibroblasts in renal fibrogenesis. Identifying the cellular origin of myofibroblasts and the key regulatory pathways that drive myofibroblast proliferation and transdifferentiation as well as capillary rarefaction is the first step to developing novel anti-fibrotic therapeutics to slow or even reverse CKD progression and ultimately reduce the prevalence of ESRD. This review will summarize recent findings concerning the cellular source of myofibroblasts and highlight recent discoveries concerning the key regulatory signaling pathways that drive their expansion and progression in CKD.
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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.