ReviewBiomolecules2019
Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments.
Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.
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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.
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Who cites it
176 citing papers in PubMed, 318 citations in OpenAlex.
- TNFα and endothelial IL-1 receptor signaling drive peritubular capillary regression and mature collagen accumulation in obstructive kidney injury.American journal of physiology. Renal physiology · 2026Article
- Article
- Pre-treatment with 2-mercaptoethanol attenuates ferroptosis-associated redox imbalance and inflammatory responses, but not tubulointerstitial fibrosis, in unilateral ureteral obstruction.Pharmacological reports : PR · 2026Article
- Peroxisomal Degradation Correlates with the Progression of Kidney Injury in a UUO Mouse Model.Biology · 2026Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- 6-gingerol attenuates renal interstitial fibrosis by downregulating PI3K/Akt/mTOR signaling pathway in unilateral ureteral obstruction rats.Scientific reports · 2026Article
- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.Biology direct · 2026Article
- Fibrosis-memory is mediated by IL-3-producing T cells and drives progression of fibrosis.The Journal of clinical investigation · 2026Article
- Resolving Inflammation in CKD: The Potential of SPMs and Omega-3 Derivatives as Biomarkers and Therapeutics.Biomedicines · 2026Review
- LYVE1 ectodomain shedding blunts lymphatic transmigration and clearance of macrophages during kidney injury.JCI insight · 2026Article
- Article
- Risedronate attenuates renal fibrosis by targeting prenylation-dependent RhoA/ROCK1 and ERK/NF-κB signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Selective blockade of latent TGF-β1 activation suppresses tissue fibrosis with good safety.Communications medicine · 2026Article
- Two-step postoperative ultrasound for early detection of ureteral obstruction after benign hysterectomy.BMC women's health · 2026Article
- Epigenetic Suppression of RASAL1 by HDAC3 and Cofactor YY1 Promotes Fibroblast-Myofibroblast Transition and Renal Fibrosis.Research (Washington, D.C.) · 2026Article
- Type IV Collagen-Targeting Nanoparticles for Efficient Delivery to the Renal Interstitium in Fibrotic Kidneys.Current drug delivery · 2026Article
- Preclinical approaches to studying liver and kidney fibrosis: models and methodologies.Frontiers in pharmacology · 2026Review
- Interpretable Machine Learning Identifies Hub Biomarkers of Renal Fibrosis and Their Potential Medical Applications.Drug design, development and therapy · 2026Article
- Multi-omics analysis to identify the dynamic changes of immune cells and marker genes in renal fibrosis.Frontiers in genetics · 2026Article
116 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
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis is the common pathway for most forms of progressive renal disease. The Unilateral Ureteral Obstruction (UUO) model is used to cause renal fibrosis, where the primary feature of UUO is tubular injury as a result of obstructed urine flow. Furthermore, experimental UUO in rodents is believed to mimic human chronic obstructive nephropathy in an accelerated manner. Renal fibrosis is the common pathway for most forms of progressive renal disease. Removing the obstruction may not be sufficient to reverse fibrosis, so an accompanying treatment may be of benefit. In this review, we have done a revision on treatments shown to ameliorate fibrosis in the context of the UUO experimental model. The treatments inhibit the production of fibrotic and inflammatory proteins such as Transforming Growth Factor β1 (TGF-β₁), Tumor Necrosis Factor α (TNF-α), collagen and fibronectin, Heat Shock Protein 47 (HSP47), suppress the proliferation of fibroblasts, prevent epithelial-to-mesenchymal transition, reduce oxidative stress, inhibit the action of the Nuclear Factor κB (NF-κB), reduce the phosphorylation of mothers against decapentaplegic homolog (SMAD) family members 2 and 3 (Smad2/3) or Mitogen-Activated Protein Kinases (MAPKs), inhibit the activation of the renin-angiotensin system. Summaries of the UUO experimental methods and alterations observed in the UUO experiments are included.
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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.