ArticleCell cycle (Georgetown, Tex.)2019
IDO1 depletion induces an anti-inflammatory response in macrophages in mice with chronic viral myocarditis.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
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- Metabolic characterization of tumor-immune interactions by multiplexed immunofluorescence reveals spatial mechanisms of immunotherapy response in non-small cell lung carcinoma (NSCLC).Nature communications · 2026Article
- The tryptophan-kynurenine pathway in cardiovascular diseases: mechanistic insights and therapeutic opportunities.Frontiers in cardiovascular medicine · 2026Review
- Integrated dual transcriptome sequencing and experimental validation reveal potential mechanisms of baicalin againstFrontiers in microbiology · 2026Article
- Anti-inflammatory myeloid angiogenic cells (MIL4-MACs) attenuate angiotensin II‒induced heart failure in mice.Scientific reports · 2025Article
- PTPN2 Negatively Regulates Macrophage Immune Responses and Cellular Bioenergetics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Anti-Inflammatory Activity of Cell-Penetrating Peptide Nucleic Acids Targeting Indoleamine 2,3-Dioxygenase 1 in IFNγ-Treated Human Keratinocytes.Biomolecules & therapeutics · 2025Article
- Comparison of moderate-intensity continuous training and high-intensity interval training effects on the Ido1-KYN-Ahr axis in the heart tissue of rats with occlusion of the left anterior descending artery.Scientific reports · 2023Article
- A tryptophan metabolite prevents depletion of circulating endothelial progenitor cells in systemic low-grade inflammation.Frontiers in immunology · 2023Article
- Bioinformatics insights into the genes and pathways on severe COVID-19 pathology in patients with comorbidities.Frontiers in physiology · 2022Article
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- Indoleamine 2,3-dioxygenase 1 limits hepatic inflammatory cells recruitment and promotes bile duct ligation-induced liver fibrosis.Cell death & disease · 2021Article
- Serum Lactate Dehydrogenase Level as a Prognostic Factor for COVID-19: A Retrospective Study Based on a Large Sample Size.Frontiers in medicine · 2021Article
- Cardiomyopathies in China: A 2018-2019 state-of-the-art review.Chronic diseases and translational medicine · 2020Review
- Indoleamine 2,3-Dioxygenase Regulates Macrophage Recruitment, Polarization and Phagocytosis in Aspergillus Fumigatus Keratitis.Investigative ophthalmology & visual science · 2020Article
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Inflammation and myocardial weakness, two major hallmarks of chronic viral myocarditis (VMC), often lead to dilated cardiomyopathy or chronic heart failure. It has been reported that indoleamine 2,3-dioxygenase-1 (IDO1) may play a pathogenic role in the progression of inflammatory diseases. Hence, the study is set out to investigate the potential role of IDO1 in chronic VMC by establishing a mouse model of VMC by intraperitoneally injected with coxsackievirus B3 (CVB3). After model establishment, the expression of IDO1 was determined by RT-qPCR and Western blot analysis. IDO1 was identified as an up-regulated gene in CVB3-induced VMC. Then, in order to elucidate the potential role of IDO1 in VMC, macrophages were isolated and treated with the overexpression plasmid of IDO1 or IDO1 inhibitor (1-MT). After that, these transfected macrophages were co-cultured with normal cardiomyocytes, followed by measurement of inflammatory factors and evaluation of cardiomyocyte injury. The overexpression of IDO1 was observed to significantly enhance the levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α), as well as lactate dehydrogenase (LDH) activity and malondialdehyde (MDA) content. By contrast, the treatment of 1-MT in macrophages reversed the promoting effects of IDO1 on cardiomyocyte injury. Co-culture experiment showed that overexpressed IDO1 impaired cardiomyocyte, which was alleviated upon treatment of 1-MT. Taken together, the key findings of the present study provide evidence that 1-MT-mediated IDO1 suppression could potentially reduce inflammatory response in macrophages and consequently ameliorate cardiomyocyte injury in mice with VMC.
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