ArticleCell death and differentiation2016
Tissue damage negatively regulates LPS-induced macrophage necroptosis.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 98 citations in OpenAlex.
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Targeting macrophage ferritin heavy chain mitigates ferroptosis and lung injury in experimental acute respiratory distress syndrome.Nature communications · 2026Article
- Article
- Tonsil‑derived mesenchymal stem cell‑derived extracellular vesicles suppress MAPK‑NF‑κB signaling and restore osteogenic differentiation in LPS‑stimulated periodontal ligament fibroblasts.Molecular medicine reports · 2026Article
- Targeted deletion of macrophage ferritin heavy chain protects from macrophage ferroptosis in acute respiratory distress syndrome.Research square · 2026Article
- Circulating and Respiratory Biomarkers in Sepsis-Induced ARDS: Diagnostic and Prognostic Insights - A Narrative Review.Journal of inflammation research · 2026Review
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- Roflumilast prevented tissue damage caused by lipopolysaccharide-induced sepsis via anti-inflammatory action.PloS one · 2026Article
- Protein arginine methylation regulates anti-inflammatory programming in response to aging stress.iScience · 2025Article
- Chondrocyte lysates activate NLRP3 inflammasome-induced pyroptosis in synovial fibroblasts to exacerbate knee synovitis by downregulating caveolin-1.Arthritis research & therapy · 2025Article
- HMGB1: new biomarker and therapeutic target of autoimmune and autoinflammatory skin diseases.Frontiers in immunology · 2025Review
- Necroptosis contributes to deoxynivalenol-induced liver injury and inflammation in weaned piglets.Journal of animal science and biotechnology · 2024Article
- Monocyte-Derived Macrophages Induce Alveolar Macrophages Death via TNF-α in Acute Lung Injury.Immunity, inflammation and disease · 2024Article
- Extracellular vesicles containing MFGE8 from colorectal cancer facilitate macrophage efferocytosis.Cell communication and signaling : CCS · 2024Article
- Propofol improves survival in a murine model of sepsis via inhibiting Rab5a-mediated intracellular trafficking of TLR4.Journal of translational medicine · 2024Article
- Dynamic mRNA network profiles in macrophages challenged with lipopolysaccharide.American journal of translational research · 2024Article
- Neutrophil extracellular traps contribute to immunothrombosis formation via the STING pathway in sepsis-associated lung injury.Cell death discovery · 2023Article
- Vemurafenib inhibits necroptosis in normal and pathological conditions as a RIPK1 antagonist.Cell death & disease · 2023Article
- Irisin attenuates acute lung injury by suppressing the pyroptosis of alveolar macrophages.International journal of molecular medicine · 2023Article
- Acute respiratory distress syndrome heterogeneity and the septic ARDS subgroup.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Infection is a common clinical complication following tissue damage resulting from surgery and severe trauma. Studies have suggested that cell pre-activation by antecedent trauma/tissue damage profoundly impacts the response of innate immune cells to a secondary infectious stimulus. Cell necroptosis, a form of regulated inflammatory cell death, is one of the mechanisms that control cell release of inflammatory mediators from important innate immune executive cells such as macrophages (Mφ), which critically regulate the progress of inflammation. In this study, we investigated the mechanism and role of trauma/tissue damage in the regulation of LPS-induced Mφ necroptosis using a mouse model simulating long-bone fracture. We demonstrate that LPS acting through Toll-like receptor (TLR) 4 promotes Mφ necroptosis. However, necroptosis is ameliorated by high-mobility group box 1 (HMGB1) release from damaged tissue. We show that HMGB1 acting through cell surface receptor for advanced glycation end products (RAGE) upregulates caveolin-1 expression, which in turn induces caveolae-mediated TLR4 internalization and desensitization to decrease Mφ necroptosis. We further show that RAGE-MyD88 activation of Cdc42 and subsequent activation of transcription factor Sp1 serves as a mechanism underlying caveolin-1 transcriptional upregulation. These results reveal a previous unidentified protective role of damage-associated molecular pattern (DAMP) molecules in restricting inflammation in response to exogenous pathogen-associated molecular pattern molecules.
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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.