ArticleMolecular medicine reports2021
Role of indoleamine 2,3-dioxygenase in ischemia-reperfusion injury of renal tubular epithelial cells.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease.Nature reviews. Nephrology · 2026Review
- Potential role of AhR in ischemia‑reperfusion injury and cancers: Focus on ferroptosis and lipid peroxidation signaling pathways (Review).International journal of molecular medicine · 2025Review
- Ferroptosis mediated by the IDO1/Kyn/AhR pathway triggers acute thymic involution in sepsis.Cell death & disease · 2025Article
- The landscape of research on ferroptosis under hypoxic conditions: a bibliometric analysis.Frontiers in pharmacology · 2025Review
- Review
- Interstitial Foci Expression of Indoleamine 2,3-Dioxygenase 1: A Potential Biomarker for Kidney Transplant Rejection.Journal of clinical medicine · 2024Article
- Comprehensive overview of the role of mitochondrial dysfunction in the pathogenesis of acute kidney ischemia-reperfusion injury: a narrative review.Journal of Yeungnam medical science · 2024Article
- Molecular Mechanisms of Oxidative Stress in Acute Kidney Injury: Targeting the Loci by Resveratrol.International journal of molecular sciences · 2023Review
- Indoleamine 2,3-Dioxygenase 1 (IDO1) in Kidney Transplantation: A Guardian against Rejection.Journal of clinical medicine · 2023Article
- The multifaceted roles of activating transcription factor 3 (ATF3) in inflammatory responses - Potential target to regulate neuroinflammation in acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
- The Road from AKI to CKD: Molecular Mechanisms and Therapeutic Targets of Ferroptosis.Cell death & disease · 2023Review
- Review
- Targeting Ferroptosis as a Promising Therapeutic Strategy for Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2022Review
- Inhibition of Malate Dehydrogenase-2 Protects Renal Tubular Epithelial Cells from Anoxia-Reoxygenation-Induced Death or Senescence.Biomolecules · 2022Article
- Puerarin Induces Molecular Details of Ferroptosis-Associated Anti-Inflammatory on RAW264.7 Macrophages.Metabolites · 2022Article
- Indoleamine 2,3 Dioxygenase 1-The Potential Link between the Innate Immunity and the Ischemia-Reperfusion-Induced Acute Kidney Injury?International journal of molecular sciences · 2022Review
- Biological Characteristics and Predictive Model of Biopsy-Proven Acute Rejection (BPAR) After Kidney Transplantation: Evidences of Multi-Omics Analysis.Frontiers in genetics · 2022Article
- CCN2 Aggravates the Immediate Oxidative Stress-DNA Damage Response following Renal Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Article
- The Role of Indoleamine 2,3-Dioxygenase in Renal Tubular Epithelial Cells Senescence under Anoxia or Reoxygenation.Biomolecules · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study evaluated indoleamine 2,3‑dioxygenase 1 (IDO) kinetics and how it affects cell survival during the two distinct phases of ischemia‑reperfusion (I‑R) injury. Primary renal proximal tubular epithelial cells (RPTECs) were cultured under anoxia or reoxygenation with or without the IDO inhibitor 1‑DL‑methyltryptophan, the aryl‑hydrocarbon receptor (AhR) inhibitor CH223191 or the ferroptosis inhibitor α‑tocopherol. Using cell imaging, colorimetric assays, PCR and western blotting, it was demonstrated that IDO was upregulated and induced apoptosis during anoxia. The related molecular pathway entails tryptophan degradation, general control non‑derepressible‑2 kinase (GCN2K) activation, increased level of phosphorylated eukaryotic translation initiation factor 2α, activating transcription factor (ATF)4, ATF3, C/EBP homologous protein, phosphorylated p53, p53, Bax, death receptor‑5 and eventually activated cleaved caspase‑3. Reoxygenation also upregulated IDO, which, in this case, induced ferroptosis. The related molecular pathway encompasses kynurenine production, AhR activation, cytochrome p450 enzymes increase, reactive oxygen species generation and eventually ferroptosis. In conclusion, in RPTECs, both anoxia and reoxygenation upregulated IDO, which in turn induced GCN2K‑mediated apoptosis and AhR‑mediated ferroptosis. Since both phases of I‑R injury share IDO upregulation as a common point, its inhibition may prove a useful therapeutic strategy for preventing or attenuating I‑R injury.
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