ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2014
Therapeutic effects of suppressors of cytokine signaling in diabetic nephropathy.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Circulating exosomal miR-16-5p and let-7e-5p are associated with bladder fibrosis of diabetic cystopathy.Scientific reports · 2024Article
- JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023Review
- Integrated bioinformatics analysis reveals novel key biomarkers in diabetic nephropathy.SAGE open medicine · 2022Article
- Review
- Exploring the mechanisms underlying the therapeutic effect of Salvia miltiorrhiza in diabetic nephropathy using network pharmacology and molecular docking.Bioscience reports · 2021Article
- miR-150-Based RNA Interference Attenuates Tubulointerstitial Fibrosis through the SOCS1/JAK/STAT PathwayMolecular therapy. Nucleic acids · 2020Article
- Current Knowledge of IL-6 Cytokine Family Members in Acute and Chronic Kidney Disease.Biomedicines · 2019Review
- SOCS1-targeted therapy ameliorates renal and vascular oxidative stress in diabetes via STAT1 and PI3K inhibition.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway.Molecular medicine reports · 2017Article
- T2DiACoD: A Gene Atlas of Type 2 Diabetes Mellitus Associated Complex Disorders.Scientific reports · 2017Article
- Suppressor of Cytokine Signaling-1 Peptidomimetic Limits Progression of Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Article
- Anti-OSM Antibody Inhibits Tubulointerstitial Lesion in a Murine Model of Lupus Nephritis.Mediators of inflammation · 2017Article
- HMGB1 is activated in type 2 diabetes mellitus patients and in mesangial cells in response to high glucose.International journal of clinical and experimental pathology · 2015Article
- JAK inhibition and progressive kidney disease.Current opinion in nephrology and hypertension · 2015Review
- Role of TGF-β1/p38 MAPK pathway in hepatitis B virus-induced tubular epithelial-myofibroblast transdifferentiation.International journal of clinical and experimental pathology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is an important pathophysiological mechanism in diabetic nephropathy (DN). Tubular epithelial cell-myofibroblast transdifferentiation (TEMT), which can be induced by many cytokines, is an important event in DN. Oncostatin M (OSM), an inflammatory cytokine, can induce TEMT in vitro. The suppressors of cytokine signaling (SOCS) proteins are negative-feedback regulators of cytokine signaling. The purpose of this study was to investigate the role of SOCS in DN. The results demonstrated that overexpression of SOCS ameliorated proteinuria, the expression of α-SMA and OSM in tubular epithelial cells, and interstitial extracellular matrix accumulation in the renal tissue of CD-1 mice. In addition, our previous studies indicated that OSM induced TEMT by activating the JAK/STAT pathway, which could be inhibited by SOCS. These results indicate that overexpression of SOCS has a therapeutic effect in DN.
Indexed as
Identifiers
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.