ReviewCurrent opinion in nephrology and hypertension2015
JAK inhibition and progressive kidney disease.
Review in Current opinion in nephrology and hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
61 citing papers in PubMed, 121 citations in OpenAlex.
- JAK1/JAK2 inhibition by baricitinib in diabetic kidney disease: results from a Phase 2 randomized controlled clinical trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018Trial
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- Review
- Amelioration of doxorubicin-mediated nephrotoxicity through antioxidant and anti-apoptotic mechanisms of 5,4'-dihydroxy-6,8-dimethoxy-7-O-rhamnosylflavone.Molecular and cellular biochemistry · 2026Article
- Podocyte-Specific Deletion of STAT3 in Krüppel-Like Factor 4-Related Experimental Podocytopathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Cytokine-Driven Janus Kinase Signal Transducer and Activator of Transcription Pathway Hyperactivity Predicts Disease Severity in Pediatric FSGS.Kidney360 · 2026Article
- Causal relationships of Janus kinase 2 with chronic kidney diseases: a two-sample Mendelian randomisation study.Clinical and experimental nephrology · 2026Article
- JAK3 Staining and CD68+ Macrophage Counts Are Increased in Patients with IgA Nephropathy.Diagnostics (Basel, Switzerland) · 2026Article
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Y665F variant of mouse Stat5b protects against acute kidney injury through transcriptomic shifts in renal gene expression.Scientific reports · 2025Article
- Multi-omic and spatial analysis of mouse kidneys highlights sex-specific differences in gene regulation across the lifespan.Nature genetics · 2025Article
- Advances and challenges in kidney fibrosis therapeutics.Nature reviews. Nephrology · 2025Review
- Butyrolactone I blocks the transition of acute kidney injury to chronic kidney disease in mice by targeting JAK1.MedComm · 2025Article
- Exploring Adiposity and Chronic Kidney Disease: Clinical Implications, Management Strategies, Prognostic Considerations.Medicina (Kaunas, Lithuania) · 2024Review
- Isoliquiritigenin attenuates high glucose-induced proliferation, inflammation, and extracellular matrix deposition in glomerular mesangial cells by suppressing JAK2/STAT3 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Integrated UPLC-ESI-MS/MS, network pharmacology, and transcriptomics to reveal the material basis and mechanism of Schisandra chinensis Fruit Mixture against diabetic nephropathy.Frontiers in immunology · 2024Article
- SOCS1 Peptidomimetic Alleviates Glomerular Inflammation in MsPGN by Inhibiting Macrophage M1 Polarization.Inflammation · 2023Article
- Comprehensive analysis of the relationship between xanthine oxidoreductase activity and chronic kidney disease.iScience · 2023Article
- Novel Therapies inKidney international reports · 2023Review
1 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewTo review the role of Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling in the progression of chronic kidney diseases. RECENT
findingsThe JAK-STAT pathway transmits signals from extracellular ligands, including many cytokines and chemokines. While these responses are best characterized in lymphoid cells, they also occur in kidney cells such as podocytes, mesangial cells, and tubular cells. JAK-STAT expression and signaling abnormalities occur in humans and animal models of different chronic kidney diseases. Enhanced expression and augmented activity of JAK1, JAK2, and STAT3 promote diabetic nephropathy and their inhibition appears to reduce the disease. Activation of JAK-STAT signaling in autosomal dominant polycystic kidney disease may play an important role in cyst growth. Activation of JAK-STAT signaling promotes HIV-associated nephropathy and may also participate in the tubular responses to chronic obstructive uropathy. On the basis of data from experimental models, inhibition of JAK-STAT signaling, via increased expression of the suppressors of cytokine signaling proteins or pharmacologic inhibition of JAK and STAT proteins, could play a therapeutic role in multiple chronic kidney diseases. SUMMARY: Activation of the JAK-STAT pathway appears to play a role in the progression of some chronic kidney diseases. More work is needed to determine the specific role the pathway plays in individual diseases.
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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 Socratic graph.