ReviewMolecular medicine (Cambridge, Mass.)2025
Targeting NINJ1-mediated cell rupture to treat inflammatory diseases.
Review in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Regulated cell death-induced coagulation dysfunction in sepsis.Journal of thrombosis and thrombolysis · 2026Review
- Time-Course Transcriptomic Analysis Reveals PANoptosis-CCL2 Axis in Herpes Simplex Keratitis.Investigative ophthalmology & visual science · 2026Article
- Ninjurin1 in cardiovascular and vascular biology: From molecular mechanisms to therapeutic opportunities.Clinical and translational medicine · 2026Review
- Research Progress of Nerve Injury-Induced Protein 1 in Cardiovascular Diseases.Cardiology research and practice · 2026Review
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- Gouty inflammation: genetic mechanisms towards flare therapy.Current opinion in rheumatology · 2025Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Cell death can terminate in plasma membrane rupture to release potent pro-inflammatory intracellular contents thereby contributing to inflammatory diseases. Cell rupture is an active process, mediated by the membrane protein ninjurin-1 (NINJ1) in pyroptosis, post-apoptosis lysis, ferroptosis, and forms of necrosis. Once activated, NINJ1 clusters into large oligomers within the membrane to initiate cellular lysis. Recent preclinical studies have demonstrated that inhibiting NINJ1 is a new strategy for treating immune-mediated diseases. Indeed, both small molecule inhibitors and neutralizing antibodies can target NINJ1 clustering to preserve plasma membrane integrity and mitigate disease pathogenesis. In this Perspective, we provide a summary of the current state of knowledge and recent developments in targeting cellular integrity during cell death through NINJ1 inhibition to treat inflammatory disease, with a focus on liver injury. As these NINJ1-mediated cell death pathways are pivotal in maintaining health and contribute to disease pathogenesis when dysregulated, the studies discussed within have broad implications across the immunologic basis of molecular medicine.
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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.