ArticleMolecular and cellular biochemistry2019
Co-treatment with interferon-γ and 1-methyl tryptophan ameliorates cardiac fibrosis through cardiac myofibroblasts apoptosis.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting canonical TGFβ/SMAD3 and ERK1/2 signaling in human valve interstitial cells to modulate immune-fibrotic responses in rheumatic heart disease.Journal of physiology and biochemistry · 2026Article
- Spironolactone and Fibrosis in Heart Failure Risk: Machine Learning Analysis of HOMAGE Trial Plasma Proteomics.MedComm · 2026Article
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
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- Review
- Causal relationship between immune cells and risk of heart failure: evidence from a Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- ABT-263 exerts a protective effect on upper urinary tract damage by alleviating neurogenic bladder fibrosis.Renal failure · 2023Article
- Regulation of cardiac fibroblasts by lymphocytes after a myocardial infarction: playing in the major league.American journal of physiology. Heart and circulatory physiology · 2023Review
- Low-dose sumatriptan improves the outcome of acute mesenteric ischemia in rats via downregulating kynurenine.Pharmacological reports : PR · 2023Article
- Effects of RAGE Deletion on the Cardiac Transcriptome during Aging.International journal of molecular sciences · 2022Article
- Multimarker profiling identifies protective and harmful immune processes in heart failure: findings from BIOSTAT-CHF.Cardiovascular research · 2022Article
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- Local Inhibition of Indoleamine 2,3-Dioxygenase Mitigates Renal Fibrosis.Biomedicines · 2021Article
- Review
- Correlation of Indoleamine-2,3-Dioxygenase and Chronic Kidney Disease: A Pilot Study.Journal of immunology research · 2021Observational
- Kynurenine Pathway Metabolites as Potential Clinical Biomarkers in Coronary Artery Disease.Frontiers in immunology · 2021Review
- Immune regulation of cardiac fibrosis post myocardial infarction.Cellular signalling · 2021Review
- The Dynamic Interplay Between Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2020Review
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac remodeling characterized by cardiac fibrosis is a pathologic process occurring after acute myocardial infarction. Fibrosis can be ameliorated by interferon-gamma (IFN-γ), which is a soluble cytokine showing various effects such as anti-fibrosis, apoptosis, anti-proliferation, immunomodulation, and anti-viral activities. However, the role of IFN-γ in cardiac myofibroblasts is not well established. Therefore, we investigated the anti-fibrotic effects of IFN-γ in human cardiac myofibroblasts (hCMs) in vitro and whether indoleamine 2,3-dioxygenase (IDO), induced by IFN-γ and resulting in cell cycle arrest, plays an important role in regulating the biological activity of hCMs. After IFN-γ treatment, cell signaling pathways and DNA contents were analyzed to assess the biological activity of IFN-γ in hCMs. In addition, an IDO inhibitor (1-methyl tryptophan; 1-MT) was used to assess whether IDO plays a key role in regulating hCMs. IFN-γ significantly inhibited hCM proliferation, and IFN-γ-induced IDO expression caused cell cycle arrest in G0/G1 through tryptophan depletion. Moreover, IFN-γ treatment gradually suppressed the expression of α-smooth muscle actin. When IDO activity was inhibited by 1-MT, marked apoptosis was observed in hCMs through the induction of interferon regulatory factor, Fas, and Fas ligand. Our results suggest that IFN-γ plays key roles in anti-proliferative and anti-fibrotic activities in hCMs and further induces apoptosis via IDO inhibition. In conclusion, co-treatment with IFN-γ and 1-MT can ameliorate fibrosis in cardiac myofibroblasts through apoptosis.
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