ArticleBMC nephrology2017
Indoleamine 2, 3-dioxygenase (IDO) increases during renal fibrogenesis and its inhibition potentiates TGF-β 1-induced epithelial to mesenchymal transition.
Article in BMC nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Single-nucleus transcriptomics illuminates sex differences during murine Escherichia coli pyelonephritis.Communications biology · 2026Article
- Single-nucleus transcriptomics illuminates sex differences during murine Escherichia coli pyelonephritis.Research square · 2025Article
- Mitigation of Ferroptosis in Diabetic Kidney Disease Through Mesenchymal Stem Cell Intervention via the Smad2/3/METTL3/S1PR1 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Gut Microbiome and Symptom Burden After Kidney Transplantation: An Overview and Research Opportunities.Biological research for nursing · 2024Review
- Article
- Decreased circulating transforming growth factor-beta (TGF-β) and kidney TGF-β immunoreactivity predict renal disease in cats with naturally occurring chronic kidney disease.Journal of feline medicine and surgery · 2023Article
- The complexity of nicotinamide adenine dinucleotide (NAD), hypoxic, and aryl hydrocarbon receptor cell signaling in chronic kidney disease.Journal of translational medicine · 2023Review
- Identification of Genetic Markers Linked to The Activity of Indoleamine 2,3-Dioxygenase and Kidney Function.Metabolites · 2023Article
- Temporal Profile of Kynurenine Pathway Metabolites in a Rodent Model of Autosomal Recessive Polycystic Kidney Disease.International journal of tryptophan research : IJTR · 2022Article
- Plasma and Urine Indoleamine 2,3-Dioxygenase Activity: Promising Biomarkers for Chronic Kidney Disease and Inflammation Status.Journal of inflammation research · 2022Article
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- Emerging Patient-Centered Concepts in Pain Among Adults With Chronic Kidney Disease, Maintenance Dialysis, and Kidney Transplant.Seminars in nephrology · 2021Review
- Transcriptomic analysis of the seminal vesicle response to the reproductive toxicant acrylamide.BMC genomics · 2021Article
- Local Inhibition of Indoleamine 2,3-Dioxygenase Mitigates Renal Fibrosis.Biomedicines · 2021Article
- The Kynurenine Pathway in Acute Kidney Injury and Chronic Kidney Disease.American journal of nephrology · 2021Review
- Correlation of Indoleamine-2,3-Dioxygenase and Chronic Kidney Disease: A Pilot Study.Journal of immunology research · 2021Observational
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIndoleamine 2, 3-dioxygenase (IDO) is an immunomodulatory molecule that has been implicated in several biological processes. Although IDO has been linked with some renal diseases, its role in renal fibrosis is still unclear. Because IDO may be modulated by TGF-β1, a potent fibrogenic molecule, we hypothesized that IDO could be involved in renal fibrosis, especially acting in the TGF-β1-induced tubular epithelial-mesenchymal transition (EMT). We analyzed the IDO expression and activity in a model of renal fibrogenesis, and the effect of the IDO inhibitor 1-methyl-tryptophan (MT) on TGF-β1-induced EMT using tubular cell culture.
methodsMale Wistar rats where submited to 7 days of UUO. Non-obstructed kidneys (CL) and kidneys from SHAM rats were used as controls. Masson's Tricrome and macrophages counting were used to chatacterize the tissue fibrosis. The EMT was analysed though immunohistochemistry and qRT-PCR. Immunohistochemestry in tissue has used to show IDO expression. MDCK cells were incubated with TGF- β1 to analyse IDO expression. Additionally, effects of TGF- β1 and the inhibition of IDO over the EMT process was acessed by immunoessays and scrath wound essay.
resultsIDO was markedly expressed in cortical and medular tubules of the UUO kidneys. Similarly to the immunolocalizaton of TGF- β1, accompanied by loss of e-cadherin expression and an increase of mesenchymal markers. Results in vitro with MDCK cells, showed that IDO was increased after stimulus with TGF-β1, and treatment with MT potentiated its expression. MDCK stimulated with TGF-β1 had higher migratory activity (scratch-wound assay), which was exacerbated by MT treatment.
conclusionsIDO is constitutively expressed in tubular cells and increases during renal fibrogenesis. Although IDO is induced by TGF-β1 in tubular cells, its chemical inhibitor acts as a profibrotic agent.
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