ArticleCells2018
Liver Immune Cells Release Type 1 Interferon Due to DNA Sensing and Amplify Liver Injury from Acetaminophen Overdose.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- Nimbolide Targeting SIRT1 Protects Against Acetaminophen-Induced Acute Liver Injury by Regulating Oxidative Stress and Endoplasmic Reticulum Stress.Pharmacology research & perspectives · 2025Article
- The crucial roles and research advances of cGAS‑STING pathway in liver diseases.Annals of medicine · 2024Review
- Transcriptotype-Driven Discovery of Apigenin as a Therapy against Cholestatic Liver Fibrosis: Through Inhibition of PANoptosis and Following Type-I Interferon Responses.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting cathepsin C ameliorates murine acetaminophen-induced liver injury.Theranostics · 2024Article
- IL-33/ST2 antagonizes STING signal transduction via autophagy in response to acetaminophen-mediated toxicological immunity.Cell communication and signaling : CCS · 2023Article
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- Mitochondria as mediators of systemic inflammation and organ cross talk in acute kidney injury.American journal of physiology. Renal physiology · 2022Review
- Emodin Attenuates Acetaminophen-Induced Hepatotoxicity via the cGAS-STING Pathway.Inflammation · 2022Article
- COMMD10 is critical for Kupffer cell survival and controls Ly6CCell reports · 2021Article
- DNA sensing and associated type 1 interferon signaling contributes to progression of radiation-induced liver injury.Cellular & molecular immunology · 2021Article
- Immune and Metabolic Alterations in Liver Fibrosis: A Disruption of Oxygen Homeostasis?Frontiers in molecular biosciences · 2021Review
- The Cytosolic DNA-Sensing cGAS-STING Pathway in Liver Diseases.Frontiers in cell and developmental biology · 2021Review
- DAMPs and sterile inflammation in drug hepatotoxicity.Hepatology international · 2019Review
- Danger-Associated Molecular Patterns (DAMPs): Molecular Triggers for Sterile Inflammation in the Liver.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
25 authors at 6 institutions in 3 countries.
Funding
Abstract
Hepatocytes may rupture after a drug overdose, and their intracellular contents act as damage-associated molecular patterns (DAMPs) that lead to additional leukocyte infiltration, amplifying the original injury. Necrosis-derived DNA can be recognized as a DAMP, activating liver non-parenchymal cells (NPCs). We hypothesized that NPCs react to DNA by releasing interferon (IFN)-1, which amplifies acetaminophen (APAP)-triggered liver necrosis. We orally overdosed different knockout mouse strains to investigate the pathways involved in DNA-mediated amplification of APAP-induced necrosis. Mice were imaged under intravital confocal microscopy to estimate injury progression, and hepatocytes and liver NPCs were differentially isolated for gene expression assays. Flow cytometry (FACS) using a fluorescent reporter mouse estimated the interferon-beta production by liver leukocytes under different injury conditions. We also treated mice with DNase to investigate the role of necrosis DNA signaling in IFN-1 production. Hepatocytes released a large amount of DNA after APAP overdose, which was not primarily sensed by these cells. However, liver NPCs promptly sensed such environmental disturbances and activated several DNA sensing pathways. Liver NPCs synthesized and released IFN-1, which was associated with concomitant hepatocyte necrosis. Ablation of IFN-1 recognition in interferon α/β receptor (IFNAR
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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 OpenQuestion graph.