ArticleThe American journal of pathology2024
Ninjurin 2 Modulates Tumorigenesis, Inflammation, and Metabolism via Pyroptosis.
Article in The American journal of pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Nerve injury-induced protein 2 preserves lysosomal membrane integrity to suppress ferroptosis.eLife · 2026Article
- Ninjurin2 Promotes Pulmonary Endothelial Barrier Dysfunction Through VEGF/VEGFR2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Ninjurins regulate hematopoietic stem cell amplification through canonical WNT signaling independent of plasma membrane rupture.Nature communications · 2026Article
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Nerve Injury-Induced Protein 2 preserves lysosomal membrane integrity to suppress ferroptosis.bioRxiv : the preprint server for biology · 2026Article
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
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- Identification of key genes underlying radiosensitivity and radioresistance in endometrial cancer through integrated bioinformatics analysis.Frontiers in genetics · 2025Article
- The Unrecognized Role of Ninjurin 2 in Inflammation, Metabolism, and Pyroptosis.The American journal of pathology · 2024Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The nerve injury-induced protein 2 (NINJ2) belongs to a family of homophilic adhesion molecules and was initially found to be involved in nerve regeneration. However, the role of NINJ2 in other cellular processes is not well studied. The Ninj2-deficient mice generated in the current study had a short lifespan and were prone to spontaneous tumors, systemic inflammation, and metabolic defects. Comprehensive carbohydrate and lipid metabolic analyses were performed to better understand the metabolic traits that contribute to these phenotypes. Carbohydrate metabolic analyses showed that NINJ2 deficiency led to defects in monosaccharide metabolism along with accumulation of multiple disaccharides and sugar alcohols. Lipidomic analyses showed that Ninj2 deficiency altered patterns of several lipids, including triglycerides, phospholipids, and ceramides. To identify a cellular process that associated with these metabolic defects, the role of NINJ2 in pyroptosis, a programmed cell death that links cancer, inflammation, and metabolic disorders, was examined. Loss of NINJ2 promoted pyroptosis by activating the NOD-like receptor protein 3 (NLRP3) inflammasome. Taken together, these data reveal a critical role of NINJ2 in tumorigenesis, inflammatory response, and metabolism via pyroptosis.
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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.