ArticleNature communications2017
NMI and IFP35 serve as proinflammatory DAMPs during cellular infection and injury.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 115 citations in OpenAlex.
- Integration of the circulating miRNome and clinical information to predict 90-day mortality in elderly COVID-19 subphenotypes.iScience · 2026Article
- Structural basis of NMI-IFP35 domains and swapping phenomenon in IFP35-NID.Journal of structural biology: X · 2026Article
- From early-onset asthma to chronic obstructive pulmonary disease: potential mediating proteins and therapeutic targets.Briefings in bioinformatics · 2026Article
- Integrated Proteomics and Metabolomics Analyses Reveal That Phosphatidylethanolamine Reprograms Macrophage Immunometabolism and Attenuates LPS-Driven Inflammation.Journal of proteome research · 2026Article
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Article
- IFI35 suppresses the transcription of hepatitis B virus cccDNA minichromosome via promoting HNF4α proteasomal degradation.Journal of biomedical science · 2026Article
- Interferon-induced protein 35 (IFI35) is associated with COVID-19 severity and clinical outcomes.Scientific reports · 2026Article
- NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates.Inflammation · 2026Article
- NMI promotes the secretion of IL-17 and exacerbates psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- NMI as a Novel pro-inflammatory Driver in Acute Pancreatitis Via PI3K-AKT Mediated Macrophage Activation.Inflammation · 2026Article
- Phillyrin promotes flap survival by mitigating pyroptosis through the TLR4/NF-κB/NLRP3 signaling pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- N-myc and STAT interactor promotes poly(I:C)-induced pulmonary coagulopathy via STAT3-dependent tissue factor.Frontiers in immunology · 2026Article
- N-myc and STAT interactor is a novel biomarker for predicting the severity and clinical outcome of sepsis: a prospective research.Frontiers in cellular and infection microbiology · 2026Article
- The role and significance of the PI3K/Akt-mTOR signaling pathway in infectious diseases.Frontiers in cellular and infection microbiology · 2026Review
- N-Myc and STAT interactor as a context-dependent switch in innate antiviral immunity.Frontiers in immunology · 2026Review
- B7 Family Molecule VSIG4 Regulates Pulmonary Anti-Influenza Immune Responses via C-Type Lectin Signal Pathway.Vaccines · 2025Article
- Multi-phase, multi-ethnic GWAS uncovers putative loci in predisposition to elite sprint and power performance, health and disease.Biology of sport · 2025Article
- IFP35, a novel DAMP, aggravates neuroinflammation following acute ischemic stroke via TLR4/NF-κB/NLRP3 signaling.Journal of neuroinflammation · 2025Article
- FXR protects against neonatal sepsis by enhancing the immunosuppressive function of MDSCs.Cellular & molecular immunology · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage-associated molecular patterns (DAMP) trigger innate immune response and exacerbate inflammation to combat infection and cellular damage. Identifying DAMPs and revealing their functions are thus of crucial importance. Here we report that two molecules, N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs and are released by activated macrophages during lipopolysaccharide-induced septic shock or acetaminophen-induced liver injury. We show that extracellular NMI and IFP35 activate macrophages to release proinflammatory cytokines by activating nuclear factor-κB through the Toll-like receptor 4 pathway. In addition, the serum levels of NMI are increased in patients who succumbed to severe inflammation. NMI deficiency reduces inflammatory responses and mortality in mouse models of sepsis and liver injury. We therefore propose that extracellular NMI and IFP35 exacerbate inflammation as DAMPs, making them potential therapeutic targets for clinical intervention.Damage-associated molecular patterns (DAMP) are important mediators of innate immunity. Here the authors show that N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs to promote inflammation by activating macrophages via the Toll-like receptor 4 and NF-κB pathways.
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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.