ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2010
Early differential expression of oncostatin M in obstructive nephropathy.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Suppression of renal crystal formation, inflammation, and fibrosis by blocking oncostatin M receptor β signaling.Scientific reports · 2024Article
- Interleukin-10 enhances recruitment of immune cells in the neonatal mouse model of obstructive nephropathy.Scientific reports · 2024Article
- Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Oncostatin M is a regulator of fibroblast growth factor 23 (FGF23) in UMR106 osteoblast-like cells.Scientific reports · 2023Article
- CCL7 as a novel inflammatory mediator in cardiovascular disease, diabetes mellitus, and kidney disease.Cardiovascular diabetology · 2022Review
- Essential roles of oncostatin M receptor β signaling in renal crystal formation in mice.Scientific reports · 2020Article
- Current Knowledge of IL-6 Cytokine Family Members in Acute and Chronic Kidney Disease.Biomedicines · 2019Review
- Oncostatin M exerts a protective effect against excessive scarring by counteracting the inductive effect of TGFβ1 on fibrosis markers.Scientific reports · 2019Article
- OSMR gene effect on the pathogenesis of chronic autoimmune Urticaria via the JAK/STAT3 pathway.Molecular medicine (Cambridge, Mass.) · 2018Article
- Anti-OSM Antibody Inhibits Tubulointerstitial Lesion in a Murine Model of Lupus Nephritis.Mediators of inflammation · 2017Article
- Synergistic induction of CCL2/MCP-1 expression driven by oncostatin M and IL-1β in human proximal tubular cells depends on STAT3 and p65 NFκB/RelA.Physiological reports · 2015Article
- Therapeutic effects of suppressors of cytokine signaling in diabetic nephropathy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
- The enigmatic cytokine oncostatin m and roles in disease.ISRN inflammation · 2013Review
- Endothelium-derived GM-CSF influences expression of oncostatin M.American journal of physiology. Cell physiology · 2011Article
- Expression of ciliary neurotrophic factor and its receptor in experimental obstructive nephropathy.Anatomy & cell biology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
Abstract
Interstitial fibrosis plays a major role in progression of renal diseases. Oncostatin M (OSM) is a cytokine that regulates cell survival, differentiation, and proliferation. Renal tissue from patients with chronic obstructive nephropathy was examined for OSM expression. The elevated levels in diseased human kidneys suggested possible correlation between OSM level and kidney tissue fibrosis. Indeed, unilateral ureteral obstruction (UUO), a model of renal fibrosis, increased OSM and OSM receptor (OSM-R) expression in a time-dependent manner within hours following UUO. In vitro, OSM overexpression in tubular epithelial cells (TECs) resulted in epithelial-myofibroblast transdifferentiation. cDNA microarray technology identified up-regulated expression of immune modulators in obstructed compared with sham-operated kidneys. In vitro, OSM treatment up-regulated CC chemokine ligand CCL7, and CXC chemokine ligand (CXCL)-14 mRNA in kidney fibroblasts. In vivo, treatment of UUO mice with neutralizing anti-OSM antibody decreased renal chemokines expression. In conclusion, OSM is up-regulated in kidney tissue early after urinary obstruction. Therefore, OSM might play an important role in initiation of renal fibrogenesis, possibly by inducing myofibroblast transdifferentiation of TECs as well as leukocyte infiltration. This process may, in turn, contribute in part to progression of obstructive nephropathy and makes OSM a promising therapeutic target in renal fibrosis.
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.