---
title: "Itaconate reduces LPS-induced septic liver injury by suppressing METs via Nrf2–ROS–PAD4 pathway"
id: "pubmed-42700231"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42700231"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42700231/"
doi: "10.1007/s00011-026-02359-7"
published_at: "2026-09-05T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Itaconate reduces LPS-induced septic liver injury by suppressing METs via Nrf2–ROS–PAD4 pathway
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42700231
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42700231/)
- **DOI:** [10.1007/s00011-026-02359-7](https://doi.org/10.1007%2Fs00011-026-02359-7)
- **Published At:** 2026-09-05T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Sepsis induces elevated levels of **macrophage extracellular traps (METs)** in liver tissue and circulation in an LPS model. - The immunometabolite **itaconate**, produced by Acod1 (Irg1), acts as a key negative regulator of MET formation. - Genetic deletion of Irg1 increased MET release, worsened hepatic injury, and decreased survival in septic mice, indicating endogenous itaconate is protective. - The itaconate derivative **4-octyl itaconate (4-OI)** markedly suppressed MET formation and improved liver injury in the LPS sepsis model. - Mechanistically, 4-OI activates the transcription factor **Nrf2**, which reduces intracellular **reactive oxygen species (ROS)**. - Reduced ROS limits activation of **peptidylarginine deiminase 4 (PAD4)**, preventing histone citrullination required for MET release. - The inhibitory effect of 4-OI on METs depends on Nrf2; absence of Nrf2 abolishes MET suppression by 4-OI, implicating an **Nrf2–ROS–PAD4** axis. - The study proposes a metabolic–immune pathway in which itaconate protects against sepsis-associated liver damage by restraining MET-mediated tissue injury via Nrf2-driven antioxidant mechanisms. - Ethical statements: animal experiments were approved by the relevant institutional committee; no human subjects were involved. - Conflict of interest: authors declared no known competing financial interests.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. * 2 Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, China. * 3 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. kaixiongtao@hust.edu.cn. * 4 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. liruidong@hust.edu.cn. # Contributed equally. * PMID: **42700231** * DOI: [ 10.1007/s00011-026-02359-7 ](https://doi.org/10.1007/s00011-026-02359-7) Item in Clipboard # Itaconate alleviates LPS-induced septic liver injury by regulating ROS-PAD4-mediated macrophages extracellular traps through Nrf2 Liwu Zeng et al. Inflamm Res. 2026. Show details Display options Display options Format Abstract PubMed PMID Inflamm Res Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Inflamm+Res%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Inflamm+Res%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) . 2026 Sep 5;75(1):204. doi: 10.1007/s00011-026-02359-7. ### Authors [Liwu Zeng](https://pubmed.ncbi.nlm.nih.gov/?term=Zeng+L&cauthor_id=42700231)[#](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-1 "Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China."), [Yaxin Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+Y&cauthor_id=42700231)[#](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-equal-contrib-explanation "Contributed equally")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-2 "Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, China."), [Gan Mao](https://pubmed.ncbi.nlm.nih.gov/?term=Mao+G&cauthor_id=42700231)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-1 "Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China."), [Yisong Gao](https://pubmed.ncbi.nlm.nih.gov/?term=Gao+Y&cauthor_id=42700231)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-1 "Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China."), [Kaixiong Tao](https://pubmed.ncbi.nlm.nih.gov/?term=Tao+K&cauthor_id=42700231)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-3 "Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. kaixiongtao@hust.edu.cn."), [Ruidong Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+R&cauthor_id=42700231)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42700231/#short-view-affiliation-4 "Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. liruidong@hust.edu.cn.") ### Affiliations * 1 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. * 2 Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, China. * 3 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. kaixiongtao@hust.edu.cn. * 4 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, Hubei Province, China. liruidong@hust.edu.cn. # Contributed equally. * PMID: **42700231** * DOI: [ 10.1007/s00011-026-02359-7 ](https://doi.org/10.1007/s00011-026-02359-7) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Activated macrophages release macrophage extracellular traps (METs), which are a major cause of tissue damage in sepsis. However, the molecular mechanisms governing their production remain poorly characterized. In this study, we demonstrate that MET levels are markedly elevated in both the liver and circulation in a lipopolysaccharide (LPS)-induced sepsis model. The immunometabolite itaconate-a product of the enzyme aconitate decarboxylase 1 (Acod1)-emerged as a critical suppressor of this pathway. Genetic ablation of immune responsive gene 1 (Irg1) resulted in heightened MET release, exacerbated hepatic injury, and decreased survival in septic mice. In contrast, the itaconate derivative 4-octyl itaconate (4-OI) robustly suppressed MET formation and ameliorated liver damage. Mechanistically, 4-OI activated the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), resulting in scavenging of intracellular reactive oxygen species (ROS), which suppressed ROS-dependent activation of peptidylarginine deiminase 4 (PAD4), thereby inhibiting histone citrullination and subsequent MET release. The suppression of MET formation by 4-OI is mediated through an Nrf2-dependent mechanism, as its absence abolishes this suppression, revealing the Nrf2-ROS-PAD4 axis's key role. The findings reveal a new metabolic-immune pathway: itaconate reduces sepsis-linked liver injury by using Nrf2 to suppress METs, suggesting a novel clinical treatment approach. **Keywords:** Itaconate; MET; Nrf2; Sepsis. © 2026. The Author(s), under exclusive licence to Springer Nature Switzerland AG. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Competing interests: The authors declare that they have no known competing financial interests. Ethics approval and consent to participate: All animal experiments conducted in this study were approved by the Animal Care and Use Committee of Tongji Medical College of Huazhong University of Science and Technology. Consent to participate: Not applicable. This research does not involve human experiments. Consent for publication: Not applicable. This research does not involve human experiments. Clinical trial number: Not applicable. ## References 1. 1. Mohus RM, Gustad LT, Damås JK, Drakesmith H. Iron-sepsis associations in population health revealed by epidemiology. EBioMedicine. 2025;120:105927. . - [DOI](https://doi.org/10.1016/j.ebiom.2025.105927) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/40957223/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/12466143/) 2. 1. Zhou HT, Huang J, Liu YK, Wang JH, Wang J. The emerging role of ferroptosis in the pathological development and progression of sepsis. Mil Med Res. 2025;12:81. . - [DOI](https://doi.org/10.1186/s40779-025-00665-5) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/41250137/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/12625605/) 3. 1. Rudd KE, Johnson SC, Agesa KM, Shackelford KA, Tsoi D, Kievlan DR, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet. 1990;395:200–11. . - [DOI](https://doi.org/10.1016/s0140-6736\(19\)32989-7) 4. 1. Elmi AN, Kwo PY. The liver in sepsis. Clin Liver Dis. 2025;29:453–67. . - [DOI](https://doi.org/10.1016/j.cld.2025.04.002) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/40670032/) 5. 1. Sun J, Zhang J, Wang X, Ji F, Ronco C, Tian J, et al. Gut-liver crosstalk in sepsis-induced liver injury. Crit Care. 2020;24:614. . - [DOI](https://doi.org/10.1186/s13054-020-03327-1) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/33076940/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/7574296/) Show all 44 references ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Carboxy-Lyases / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carboxy-Lyases%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carboxy-Lyases) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Hydro-Lyases Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Hydro-Lyases%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Hydro-Lyases) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Lipopolysaccharides Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Lipopolysaccharides%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Lipopolysaccharides) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Liver / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Liver) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Liver / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Liver) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Liver / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver%2Fpathology%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Liver) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Liver Diseases* / drug therapy Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver+Diseases%2Fdrug+therapy%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Liver+Diseases) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42700231/) * Liver Diseases* / etiology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver+Diseases%2Fetiology%22%5BMAJ
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