ArticleESC heart failure2023
Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction.
Article in ESC heart failure, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 35 citations in OpenAlex.
- The Role of Aryl Hydrocarbon Receptor-Dependent Signaling Pathway in the Profibrotic Effects of Dioxin-like Compounds in Human Renal Tubular Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Salvianolic acid B protects cardiac function via β3-AR/miRNA-1 axis-mediated cardiomyocyte proliferation in myocardial infarction rats.American journal of translational research · 2026Article
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- An Integrated Analysis of Transcriptomics and Metabolomics Elucidates the Role and Mechanism of TRPV4 in Blunt Cardiac Injury.Metabolites · 2025Article
- Exploring the Potential Effects and Mechanism of Astragalus Membranaceus in Treating Ischemic Heart Failure Based on Network Pharmacology and Experimental Verification.Combinatorial chemistry & high throughput screening · 2025Article
- RING finger protein 5 protects against acute myocardial infarction by inhibiting ASK1.BMC cardiovascular disorders · 2024Article
- Modulation of anti-cardiac fibrosis immune responses by changing M2 macrophages into M1 macrophages.Molecular medicine (Cambridge, Mass.) · 2024Article
- Inhibition of tartrate-resistant acid phosphatase 5 can prevent cardiac fibrosis after myocardial infarction.Molecular medicine (Cambridge, Mass.) · 2024Article
- Synergistic combinations ofFrontiers in pharmacology · 2024Article
- Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction.ESC heart failure · 2023Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
aimsLeft ventricular remodelling subsequent to myocardial infarction (MI) constitutes a pivotal underlying cause of heart failure. Intervention with the nontoxic endogenous aryl hydrocarbon receptor (AHR) agonist 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) in the acute phase of MI has been shown to ameliorate cardiac function, but its role in the chronic phase remains obscured. This study explores the beneficial role of ITE in delaying the progression of heart failure in the chronic phase of MI. METHODS AND
resultsMI rats established by ligating the left anterior descending coronary artery were treated with the indicated concentration of the AHR agonist ITE or vehicle alone. Echocardiography was performed to determine cardiac structure and function; myocardial morphology and fibrosis were observed by haematoxylin and eosin and Masson's trichrome staining; serum biochemical indices, BNP, and inflammatory cytokine levels were detected by enzyme-linked immunosorbent assay; F4/80
conclusionsThe AHR agonist ITE alleviates cardiomyocyte apoptosis through the Akt/p70S6K signalling pathway, thereby rescuing left ventricular adverse remodelling and cardiac dysfunction after MI.
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