ReviewFrontiers in physiology2016
Role of Bone Marrow-Derived Fibroblasts in Renal Fibrosis.
Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 44 citations in OpenAlex.
- Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Integrated network pharmacology and experimental validation to investigate the therapeutic effects and mechanisms of SJZT on hypertensive nephropathy.Frontiers in pharmacology · 2025Article
- Multi-organ single-cell RNA sequencing in mice reveals early hyperglycemia responses that converge on fibroblast dysregulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- JMJD3 ablation in myeloid cells confers renoprotection in mice with DOCA/salt-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches.International journal of molecular sciences · 2022Review
- Wound healing, fibroblast heterogeneity, and fibrosis.Cell stem cell · 2022Review
- Pharmacological Inhibition of STING/TBK1 Signaling Attenuates Myeloid Fibroblast Activation and Macrophage to Myofibroblast Transition in Renal Fibrosis.Frontiers in pharmacology · 2022Article
- Jmjd3/IRF4 axis aggravates myeloid fibroblast activation and m2 macrophage to myofibroblast transition in renal fibrosis.Frontiers in immunology · 2022Article
- Detection of infiltrating fibroblasts by single-cell transcriptomics in human kidney allografts.PloS one · 2022Article
- Myeloid PTEN deficiency aggravates renal inflammation and fibrosis in angiotensin II-induced hypertension.Journal of cellular physiology · 2022Article
- Article
- Shifting Paradigms for Suppressing Fibrosis in Kidney Transplants: Supplementing Perfusion Solutions With Anti-fibrotic Drugs.Frontiers in medicine · 2021Review
- Phosphoinositide 3-kinase γ deficiency attenuates kidney injury and fibrosis in angiotensin II-induced hypertension.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020Article
- Differential Urinary Proteome Analysis for Predicting Prognosis in Type 2 Diabetes Patients with and without Renal Dysfunction.International journal of molecular sciences · 2020Article
- Article
- Fibrocytes, Wound Healing, and Corneal Fibrosis.Investigative ophthalmology & visual science · 2020Review
- Disruption of CXCR6 Ameliorates Kidney Inflammation and Fibrosis in Deoxycorticosterone Acetate/Salt Hypertension.Scientific reports · 2020Article
- The Significance of NOTCH Pathway in the Development of Fibrosis in Systemic Sclerosis.Annals of dermatology · 2019Review
- Long term safety of targeted internalization of cell penetrating peptide crotamine into renal proximal tubular epithelial cells in vivo.Scientific reports · 2019Article
- microRNA Crosstalk Influences Epithelial-to-Mesenchymal, Endothelial-to-Mesenchymal, and Macrophage-to-Mesenchymal Transitions in the Kidney.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Renal fibrosis represents a common pathway leading to progression of chronic kidney disease. Renal interstitial fibrosis is characterized by extensive fibroblast activation and excessive production and deposition of extracellular matrix (ECM), which leads to progressive loss of kidney function. There is no effective therapy available clinically to halt or even reverse renal fibrosis. Although activated fibroblasts/myofibroblasts are responsible for the excessive production and deposition of ECM, their origin remains controversial. Recent evidence suggests that bone marrow-derived fibroblast precursors contribute significantly to the pathogenesis of renal fibrosis. Understanding the molecular signaling mechanisms underlying the recruitment and activation of the bone marrow-derived fibroblast precursors will lead to novel therapy for the treatment of chronic kidney disease. In this review, we summarize recent advances in our understanding of the recruitment and activation of bone marrow-derived fibroblast precursors in the kidney and the development of renal fibrosis and highlights new insights that may lead to novel therapies to prevent or reverse the development of renal 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.