ArticleFrontiers in pharmacology2017
Progression of Tubulointerstitial Fibrosis and the Chronic Kidney Disease Phenotype - Role of Risk Factors and Epigenetics.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis 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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Pooled it
- Endotrophin is a risk marker of complications in CANagliflozin cardioVascular Assessment Study (CANVAS): a randomized controlled trial.Cardiovascular diabetology · 2022Trial
- 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
- Characterization and classification of chronic kidney disease by spatial MIST and deep learning algorithm.American journal of physiology. Renal physiology · 2025Article
- Review
- Collagen V regulates renal function after kidney injury and can be pharmacologically targeted to enhance kidney repair in mice.Science translational medicine · 2025Article
- Kidney Fibrosis In Vitro and In Vivo Models: Path Toward Physiologically Relevant Humanized Models.Advanced healthcare materials · 2025Review
- Sulforaphane Restores Mitochondrial β-Oxidation and Reduces Renal Lipid Accumulation in a Model of Releasing Unilateral Ureteral Obstruction.Antioxidants (Basel, Switzerland) · 2025Article
- Long term outcomes of patients with chronic kidney disease after COVID-19 in an urban population in the Bronx.Scientific reports · 2025Article
- Metabolite pathway alterations identified by magnetic resonance metabolomics in a proximal tubular epithelial cell line treated with TGF-β1.Physiological reports · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Baicalin: a potential therapeutic agent for acute kidney injury and renal fibrosis.Frontiers in pharmacology · 2025Review
- Therapeutic potential ofInternational journal of medical sciences · 2025Article
- The impact of GLP-1 receptor agonist liraglutide on blood pressure profile, hydration, natriuresis in diabetic patients with severely impaired kidney function.Scientific reports · 2024Article
- Kidney Fibrosis and Oxidative Stress: From Molecular Pathways to New Pharmacological Opportunities.Biomolecules · 2024Review
- Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis.Physiological reviews · 2023Review
- Novel Model of Oxalate Diet-Induced Chronic Kidney Disease in Dahl-Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Pyruvate kinase M2 modification by a lipid peroxidation byproduct acrolein contributes to kidney fibrosis.Frontiers in medicine · 2023Article
- Artificial Intelligence-Assisted Renal Pathology: Advances and Prospects.Journal of clinical medicine · 2022Review
- Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies.International journal of molecular sciences · 2022Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the kidney has capacity to repair after mild injury, ongoing or severe damage results in scarring (fibrosis) and an associated progressive loss of kidney function. However, despite its universal significance, evidence highlights a population based heterogeneity in the trajectory of chronic kidney disease (CKD) in these patients. To explain the heterogeneity of the CKD phenotype requires an understanding of the relevant risk factors for fibrosis. These factors include both the extrinsic nature of injury, and intrinsic factors such as age, gender, genetics, and perpetual activation of fibroblasts through priming. In many cases an additional level of regulation is provided by epigenetic mechanisms which integrate the various pro-fibrotic and anti-fibrotic triggers in fibrogenesis. In this review we therefore examine the various molecular and structural changes of fibrosis, and how they are influenced by extrinsic and intrinsic factors. Our aim is to provide a unifying hypothesis to help explain the transition from acute to CKD.
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What OpenQuestion holds
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.