ArticleHippokratia2009
Renal fibrosis.
Article in Hippokratia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
35 citing papers in PubMed, 33 citations in OpenAlex.
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- The PI3K-AKT-mTOR signaling pathway mediates epithelial mesenchymal transition and cytoskeletal architecture changes induce to renal fibrosis after Bisphenol S exposure.Scientific reports · 2025Article
- Nutritional content and renoprotective potential of miracle tree (Biotechnologia · 2025Review
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- Co-regulation and synteny of GFM2 and NSA2 links ribosomal function in mitochondria and the cytosol with chronic kidney disease.Molecular medicine (Cambridge, Mass.) · 2024Review
- Article
- Novel Approaches in Chronic Renal Failure without Renal Replacement Therapy: A Review.Biomedicines · 2023Review
- EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023Review
- Cell-Matrix Interactions in Renal Fibrosis.Kidney and dialysis · 2022Article
- Hormonal Regulation of Renal Fibrosis.Life (Basel, Switzerland) · 2022Review
- Abnormal Iron and Lipid Metabolism Mediated Ferroptosis in Kidney Diseases and Its Therapeutic Potential.Metabolites · 2022Review
- Targeting lysine-specific demethylase 1A inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Mechanisms of ferroptosis in chronic kidney disease.Frontiers in molecular biosciences · 2022Review
- Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Review
- Prospects for Protective Potential ofPlants (Basel, Switzerland) · 2021Review
- Acute Decompensated Heart Failure and the Kidney: Physiological, Histological and Transcriptomic Responses to Development and Recovery.Journal of the American Heart Association · 2021Article
- The promising shadow of microbubble over medical sciences: from fighting wide scope of prevalence disease to cancer eradication.Journal of biomedical science · 2021Review
- Treadmill Exercise Training Ameliorates Functional and Structural Age-Associated Kidney Changes in Male Albino Rats.TheScientificWorldJournal · 2021Article
- Microbiome, Immunosenescence, and Chronic Kidney Disease.Frontiers in medicine · 2021Review
- Progress in drug delivery system for fibrosis therapy.Asian journal of pharmaceutical sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubulointerstitial renal fibrosis, characterized as a progressive detrimental connective tissue deposition on the kidney parenchyma, appears to be a harmful process leading inevitably to renal function deterioration, independently of the primary renal disease which causes the original kidney injury. Epithelial to Mesenchymal Transition (EMT) of tubular epithelial cells which are transformed to mesenchymal fibroblasts migrating to adjacent interstitial parenchyma constitutes the principal mechanism of renal fibrosis along with local and circulating cells. Proteinuria as well as hypoxia is included among the main mechanisms of EMT stimulation. TGFbeta-1 through the SMAD pathway is considered as the main modulator regulating the EMT molecular mechanism, probably in cooperation with hypoxia inducible factors. Hepatocyte Growth Factor (HGF) and Bone Morphogenetic Factor-7 (BMF-7) are inhibitory to EMT molecules which could prevent in experimental and clinical level the catastrophic process of interstitial fibrosis. Interesting data emerge indicating that HGF and BMF-7 administration prevents the peritoneal fibrosis of mesothelial cells.
Indexed as
Identifiers
20011086PMC2776335W4300563131What 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.