ArticleCell communication and signaling : CCS2022
Macrophage Notch1 inhibits TAK1 function and RIPK3-mediated hepatocyte necroptosis through activation of β-catenin signaling in liver ischemia and reperfusion injury.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Oxidized Phospholipids Aggravate Hepatic Ischemia/Reperfusion Injury by Promoting Macrophage M1 Polarization Via Regulating the Wnt/β-catenin/Autophagy Axis.Inflammation · 2026Article
- Sterile Inflammation and Cell Death Pathways in Liver Ischemia-Reperfusion Injury: A Review and Perspective.Endocrine, metabolic & immune disorders drug targets · 2026Review
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- Article
- Notch signaling in liver diseases: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Bioinformatics analysis and experimental validation reveal that heat HSP90AA1 enhances intestinal ischemia reperfusion induced necroptosis by inducing phosphorylated MLKL.Scientific reports · 2025Article
- Feedback Loops Shape Oxidative and Immune Interactions in Hepatic Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Nuclear receptor FXR inhibits ferroptosis to alleviate hepatic ischemia-reperfusion injury by targeting GPX4 in a mouse model.Journal of molecular histology · 2025Article
- The Role and Mechanism of TRIM13 Regulation of TRAF6 Ubiquitination in the Synergy of Inflammatory Responses and Neurotoxicity Induced by METH and HIV- 1 Tat Protein in Astrocytes.Neurotoxicity research · 2025Article
- Discovery of Endothelial-Monocyte Crosstalk in Ischemic-Reperfusion Injury Following Liver Transplantation Based on Integration of Single-Cell RNA and Transcriptome RNA Sequencing.Journal of cellular and molecular medicine · 2025Article
- Exploring cell death mechanisms in liver transplantation: implications for graft survival.Frontiers in immunology · 2025Review
- Cross Talk Between Macrophages and Podocytes in Diabetic Nephropathy: Potential Mechanisms and Novel Therapeutics.Mediators of inflammation · 2025Review
- Cell Death in Liver Disease and Liver Surgery.Biomedicines · 2024Review
- Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway.International journal of biological sciences · 2024Article
- REGγ deficiency ameliorates hepatic ischemia and reperfusion injury in a mitochondrial p66shc dependent manner in mice.Translational gastroenterology and hepatology · 2024Article
- Gp78 deficiency in hepatocytes alleviates hepatic ischemia-reperfusion injury via suppressing ACSL4-mediated ferroptosis.Cell death & disease · 2023Article
- Macrophage PTEN controls STING-induced inflammation and necroptosis through NICD/NRF2 signaling in APAP-induced liver injury.Cell communication and signaling : CCS · 2023Article
- TRAF6 regulates the abundance of RIPK1 and inhibits the RIPK1/RIPK3/MLKL necroptosis signaling pathway and affects the progression of colorectal cancer.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNotch signaling is highly conserved and critically involved in cell differentiation, immunity, and survival. Activation of the Notch pathway modulates immune cell functions during the inflammatory response. However, it remains unknown whether and how the macrophage Notch1 may control the innate immune signaling TAK1, and RIPK3-mediated hepatocyte necroptosis in liver ischemia and reperfusion injury (IRI). This study investigated the molecular mechanisms of macrophage Notch1 in modulating TAK1-mediated innate immune responses and RIPK3 functions in liver IRI.
methodsMyeloid-specific Notch1 knockout (Notch1
resultsIR stress-induced Notch1 activation evidenced by increased nuclear Notch intracellular domain (NICD) expression in liver macrophages. Myeloid Notch1 deficiency exacerbated IR-induced liver damage, with increased serum ALT levels, macrophage/neutrophil accumulation, and proinflammatory cytokines/chemokines production compared to the Notch1
conclusionsMacrophage Notch1 controls TAK1-mediated innate immune responses and RIPK3-mediated hepatocyte necroptosis through activation of β-catenin. β-catenin is required for the macrophage Notch1-mediated immune regulation in liver IRI. Our findings demonstrate that the macrophage Notch1-β-catenin axis is a crucial regulatory mechanism in IR-triggered liver inflammation and provide novel therapeutic potential in organ IRI and transplant recipients. Video abstract.
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