ArticleFrontiers in immunology2021
Protective Role of Kynurenine 3-Monooxygenase in Allograft Rejection and Tubular Injury in Kidney Transplantation.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Serotonin, Kynurenine, and Indole Pathways of Tryptophan Metabolism in Humans in Health and Disease.Nutrients · 2026Review
- Review
- Kynurenine Pathway after Kidney Transplantation: Friend or Foe?International journal of molecular sciences · 2024Review
- Contribution of tryptophan and its metabolites to transplant outcome: a mini-review.Frontiers in immunology · 2024Review
- Indoleamine 2,3-Dioxygenase 1: A Promising Therapeutic Target in Malignant Tumor.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubular epithelial cells (TECs) are the primary targets of ischemia-reperfusion injury (IRI) and rejection by the recipient's immune response in kidney transplantation (KTx). However, the molecular mechanism of rejection and IRI remains to be identified. Our previous study demonstrated that kynurenine 3-monooxygenase (KMO) and kynureninase were reduced in ischemia-reperfusion procedure and further decreased in rejection allografts among mismatched pig KTx. Herein, we reveal that TEC injury in acutely rejection allografts is associated with alterations of Bcl2 family proteins, reduction of tight junction protein 1 (TJP1), and TEC-specific KMO. Three cytokines, IFN
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Registered trials
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