ReviewFrontiers in immunology2025
Multifaceted roles of ninjurin1 in immunity, cell death, and disease.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Research Progress on NINJ1-Mediated Plasma Membrane Rupture Regulation of Pathogen Infection Process.International journal of molecular sciences · 2026Review
- NINJ1 as a novel biomarker of intestinal injury in necrotizing enterocolitis.BMC pediatrics · 2026Observational
- Ninjurin1 in cardiovascular and vascular biology: From molecular mechanisms to therapeutic opportunities.Clinical and translational medicine · 2026Review
- Nerve injury promotes glial immune responses through a Draper/Ninjurin A pathway.Neurobiology of disease · 2026Article
- Research Progress of Nerve Injury-Induced Protein 1 in Cardiovascular Diseases.Cardiology research and practice · 2026Review
- Digging deeper into NINJ1: its multifaceted role in central nervous system diseases.Frontiers in immunology · 2026Review
- Uric Acid and Preeclampsia: Pathophysiological Interactions and the Emerging Role of Inflammasome Activation.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ninjurin1 (NINJ1) is initially identified as a nerve injury-induced adhesion molecule that facilitates axon growth. It is initially characterized to promote nerve regeneration and mediate the transendothelial transport of monocytes/macrophages associated with neuroinflammation. Recent evidence indicates that NINJ1 mediates plasma membrane rupture (PMR) in lytic cell death. The absence or inhibition of NINJ1 can delay PMR, thereby mitigating the spread of inflammation resulting from cell lysis and preventing the progression of various cell death-related pathologies, suggesting a conserved regulatory mechanism across these processes. Further research elucidated the structural basis and mechanism of NINJ1-mediated PMR. Although the role of NINJ1 in PMR is established, the identity of its activating factors and its implications in diseases remain to be fully explored. This review synthesizes current knowledge regarding the structural basis and mechanism of NINJ1-mediated PMR and discusses its significance and therapeutic targeting potential in inflammatory diseases, neurological disorders, cancer, and vascular injuries.
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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 Socratic graph.