ArticleInternational journal of molecular sciences2022
The Aryl Hydrocarbon Receptor Ligand FICZ Improves Left Ventricular Remodeling and Cardiac Function at the Onset of Pressure Overload-Induced Heart Failure in Mice.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Aryl hydrocarbon receptor ligand 6-formylindolo[3,2-b]carbazole attenuates pressure overload cardiac hypertrophy by activating the CYP1A1/19(S)-hydroxyeicosatetraenoic acid (HETE) and suppressing midchain-HETEs/G protein coupled receptor 31 pathways.Drug metabolism and disposition: the biological fate of chemicals · 2026Article
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- Semisupervised Contrastive Learning for Bioactivity Prediction Using Cell Painting Image Data.Journal of chemical information and modeling · 2025Article
- Benzo[Frontiers in immunology · 2023Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Adverse ventricular remodeling is the heart's response to damaging stimuli and is linked to heart failure and poor prognosis. Formyl-indolo [3,2-b] carbazole (FICZ) is an endogenous ligand for the aryl hydrocarbon receptor (AhR), through which it exerts pleiotropic effects including protection against inflammation, fibrosis, and oxidative stress. We evaluated the effect of AhR activation by FICZ on the adverse ventricular remodeling that occurs in the early phase of pressure overload in the murine heart induced by transverse aortic constriction (TAC). Cardiac structure and function were evaluated by cardiac magnetic resonance imaging (CMRI) before and 3 days after Sham or TAC surgery in mice treated with FICZ or with vehicle, and cardiac tissue was used for biochemical studies. CMRI analysis revealed that FICZ improved cardiac function and attenuated cardiac hypertrophy. These beneficial effects involved the inhibition of the hypertrophic calcineurin/NFAT pathway, transcriptional reduction in pro-fibrotic genes, and antioxidant effects mediated by the NRF2/NQO1 pathway. Overall, our findings provide new insight into the role of cardiac AhR signaling in the injured heart.
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Registered trials
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