ArticleJournal of translational medicine2023
TREM-1 triggers necroptosis of macrophages through mTOR-dependent mitochondrial fission during acute lung injury.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 61 citations in OpenAlex.
- Clinicopathological significance and prognostic value of the MSI1/MTFR2 axis in clear cell renal cell carcinoma: linking stemness and mitochondrial dynamics.Medical molecular morphology · 2026Article
- Mitochondrial Dysfunction at the Crossroads of Necroptosis: Mechanisms, Molecular Mediators, and Therapeutic Opportunities.Journal of cellular and molecular medicine · 2026Review
- Necroptosis in alveolar epithelium orchestrates lung ischemia-reperfusion injury: a multi-omics study.Respiratory research · 2026Article
- NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury.Cell death & disease · 2026Article
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications.Journal of pharmaceutical analysis · 2026Article
- MiR-100-5p is involved in severe pneumonia in children by targeting MTOR.BMC immunology · 2026Article
- Trem1 regulates neutrophil metabolism and recruitment in lung ischemia-reperfusion injury.Redox biology · 2026Article
- Triggering receptor expressed on myeloid cell family in atherosclerosis: from mechanisms to intervention strategies.Cell communication and signaling : CCS · 2026Review
- Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Impaired BCAA Catabolism Contributes To Acute Lung Injury By Triggering Oxidative Stress and Inflammatory Response Via the MAPK Pathway.Inflammation · 2026Article
- How cells die determines the consequences of tissue repair: roles of programmed cell death in lung injury on the progression of pulmonary fibrosis.Molecular and cellular biochemistry · 2026Review
- Baihe Gujin decoction ameliorates sepsis-induced acute lung injury through Nrf2/GPX4-mediated antioxidant defense and PPARα-driven metabolic reprogramming: a multi-omics investigation.Frontiers in immunology · 2026Article
- Research Prospects for Necroptosis in Inflammatory Diseases: A Bibliometric Analysis.Current medicinal chemistry · 2026Review
- The SARS-CoV-2 nucleocapsid protein induces microglia senescence-mediated cognitive impairment via Glycolysis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- Mitochondrial dysfunction triggers Zbp1-mediated necroptosis and inflammation in acute lung injury.Biomolecules & biomedicine · 2025Article
- Single-cell RNA-seq combined with bulk RNA-seq analysis identifies necroptosis-related genes as therapeutic targets for periodontitis.BMC medical genomics · 2025Article
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Double-edged mitophagy: balancing inflammation and resolution in lung disease.Clinical science (London, England : 1979) · 2025Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNecroptosis of macrophages is a necessary element in reinforcing intrapulmonary inflammation during acute lung injury (ALI). However, the molecular mechanism that sparks macrophage necroptosis is still unclear. Triggering receptor expressed on myeloid cells-1 (TREM-1) is a pattern recognition receptor expressed broadly on monocytes/macrophages. The influence of TREM-1 on the destiny of macrophages in ALI requires further investigation.
methodsTREM-1 decoy receptor LR12 was used to evaluate whether the TREM-1 activation induced necroptosis of macrophages in lipopolysaccharide (LPS)-induced ALI in mice. Then we used an agonist anti-TREM-1 Ab (Mab1187) to activate TREM-1 in vitro. Macrophages were treated with GSK872 (a RIPK3 inhibitor), Mdivi-1 (a DRP1 inhibitor), or Rapamycin (an mTOR inhibitor) to investigate whether TREM-1 could induce necroptosis in macrophages, and the mechanism of this process.
resultsWe first observed that the blockade of TREM-1 attenuated alveolar macrophage (AlvMs) necroptosis in mice with LPS-induced ALI. In vitro, TREM-1 activation induced necroptosis of macrophages. mTOR has been previously linked to macrophage polarization and migration. We discovered that mTOR had a previously unrecognized function in modulating TREM-1-mediated mitochondrial fission, mitophagy, and necroptosis. Moreover, TREM-1 activation promoted DRP1
conclusionIn this study, we reported that TREM-1 acted as a necroptotic stimulus of AlvMs, fueling inflammation and aggravating ALI. We also provided compelling evidence suggesting that mTOR-dependent mitochondrial fission is the underpinning of TREM-1-triggered necroptosis and inflammation. Therefore, regulation of necroptosis by targeting TREM-1 may provide a new therapeutic target for ALI in the future.
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