ArticleJournal of cellular and molecular medicine2024
Aryl Hydrocarbon Receptor Alleviates Hepatic Fibrosis by Inducing Hepatic Stellate Cell Ferroptosis.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Mechanistic Insights into Regulation of the Aryl Hydrocarbon Receptor Expression in Mouse and Human Hepatoma Cells.International journal of molecular sciences · 2026Article
- Tipping the balance: NRF2's dual role in ferroptotic fate.Oncogenesis · 2026Review
- Longchai Decoction Treated the Fibrosis of Liver Induced by CClJournal of cellular and molecular medicine · 2026Article
- Review
- Gut microbiota-derived metabolites and host interactions in fibrotic diseases: mechanisms, cross-organ signatures, and therapeutic opportunities.Frontiers in microbiology · 2026Review
- The role of tryptophan-AhR signaling in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD): implications for therapeutic strategies.Frontiers in immunology · 2026Review
- Aryl hydrocarbon receptor: a multifaceted environmental sensor in liver homeostasis and disease.Frontiers in medicine · 2026Review
- Aryl hydrocarbon receptor regulates programmed cell death in diseases: molecular mechanisms and therapeutic implications.Frontiers in immunology · 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
- The aryl hydrocarbon receptor in liver injury: a double-edged sword in roles, mechanisms, and future perspectives.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Liver injury-induced activation of hepatic stellate cells (HSCs) is a crucial step in the progression of liver fibrosis. The aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, is highly expressed in the liver. However, the role of AHR in liver fibrosis remains controversial. Our study revealed that the nontoxic ligand YH439 directly activated the AHR and regulated the expression of multidrug-resistant protein 1 (Mrp1) in mouse hepatic stellate cells (mHSCs), thereby diminishing the antioxidant capacity of mHSCs by promoting GSH efflux, and specifically inducing mHSCs ferroptosis without affecting hepatocytes. In a chronic liver fibrosis model, YH439 activated AHR to promote mHSC ferroptosis without causing hepatocyte ferroptosis, thereby alleviating liver fibrosis. Conclusively, this study shows that AHR alleviates liver fibrosis in mice by selectively inducing mHSC ferroptosis without causing hepatocyte ferroptosis and suggests that AHR is a potential target for the treatment of liver fibrosis.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.