ArticleJournal of inflammation research2024
Maresin1 Inhibits Ferroptosis via the Nrf2/SLC7A11/GPX4 Pathway to Protect Against Sepsis-Induced Acute Liver Injury.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
What it found
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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.
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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.
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Who cites it
11 citing papers in PubMed.
- Knockdown of PTEN Inhibits Autophagy-Dependent Ferroptosis to Alleviate LPS-Induced Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Maresin-1 Alleviates Sepsis-Induced Liver Injury by Regulating Apoptosis and Autophagy via Activation of the PI3K/Akt Signaling Pathway in Mice.Current issues in molecular biology · 2026Article
- Metabolomics and Network Pharmacology-Based Screening of Candidate Hepatoprotective Metabolites in FermentedCurrent issues in molecular biology · 2026Article
- Natural products in treating sepsis-associated lung and liver injuries by mediating ferroptosis, current progress, and future perspective.Frontiers in pharmacology · 2026Review
- Regulated cell death in sepsis-associated liver injury: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
- Targeting ferroptosis as a therapeutic strategy for hepatotoxicity.Toxicology reports · 2025Review
- Ferroptosis and macrophage efferocytosis in periodontitis: Biological insights and therapeutic advances.Virulence · 2025Review
- Alpinetin pretreatment prevents lipopolysaccharide/D-galactosamine-induced acute liver injury in mice by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 pathway.Scientific reports · 2025Article
- Ferroptosis as a key player in the pathogenesis and intervention therapy in liver injury: focusing on drug-induced hepatotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Maresin 1 Alleviates Seizure Symptoms by Modulating the Crosstalk Between Inflammation and Ferroptosis.Journal of inflammation research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Maresin 1 (MaR1) is a specialized pro-resolving mediator with anti-inflammatory properties that promotes tissue repair. This study aims to investigate the molecular involvement of MaR1 in protecting against sepsis-induced acute liver injury (SI-ALI). Methods: In vivo, a murine SI-ALI model was established using the cecal ligation and puncture (CLP) paradigm, providing a system in which the mechanistic functions of MaR1 could be tested. These analyses were supplemented through in vitro assays in which Alpha mouse liver 12 (AML12) hepatocytes and RAW264.7 macrophages were co-cultured in a Transwell system, with lipopolysaccharide (LPS) stimulation being used to establish a sepsis model. These cells were treated with MaR1 and/or nuclear factor erythroid 2-related factor 2 (Nrf2)inhibitor, while lentiviral transduction was used to knock down Nrf2 within AML12 cells. Hepatic pathological damage was assessed through hematoxylin and eosin staining. Lipid peroxidation-related analyses were conducted through the use of thiobarbituric acid, ferrous ions, glutathione, and appropriate fluorescent probes for reactive oxygen species detection. Liver enzymes and inflammatory mediators were quantified using appropriate Enzyme-Linked Immunosorbent Assays (ELISAs). Protein concentrations were evaluated via Western blot analysis. Results: The presence of ferroptosis in SI-ALI. MaR1 was found to proficiently suppress ferroptosis in SI-ALI. Mechanistically, MaR1 enhanced Nrf2 expression in AML12 hepatocytes, while the Nrf2 inhibitor ML-385 or Nrf2 siRNA mitigated MaR1's regulatory influence on ferroptosis. Meanwhile, the expressions of the downstream genes solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) diminished, suggesting that MaR1 has a protective function via activating the Nrf2/SLC7A11/GPX4 pathway to mitigate ferroptosis in septic liver injury. Conclusion: The results indicate that MaR1 mitigates SI-ALI via stimulating the Nrf2/SLC7A11/GPX4 pathway to suppress ferroptosis. Moreover, it offers significant potential as a new agent for the prevention of SI-ALI.
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