ArticleThe EMBO journal2024
NINJ1 induces plasma membrane rupture and release of damage-associated molecular pattern molecules during ferroptosis.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Emerging research themes in ferroptosis research for non-small cell lung cancer: a bibliometric and visualized analysis.Frontiers in immunology · 2025Pooled it
- NINJ1-mediated membrane rupture bridges cell death to tissue inflammation.Biochemical Society transactions · 2026Review
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- A Novel Biofilm Amyloid Ligand for Caspase-11 Drives Hyperactivation in Dendritic Cells.bioRxiv : the preprint server for biology · 2026Article
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Mechanisms underlying propagation of ferroptotic cell death.Nature cell biology · 2026Review
- Cell Type-Specific Ferroptosis Regulatory Networks in the Bone Microenvironment: Implications for the Pathogenesis and Treatment of Osteoporosis.Traffic (Copenhagen, Denmark) · 2026Review
- Bile Acid Glycochenodeoxycholic Acid (GCDCA) Might Induce the Loss of Plasma Membrane Integrity and the Release of LDH From Ovarian Granulosa Cells, With Implications in PCOS.Journal of applied toxicology : JAT · 2026Article
- Ninjurin-1 mediates hepatic ischemia-reperfusion injury.Science advances · 2026Article
- Structural and molecular principles of DAMP biology.Nature structural & molecular biology · 2026Review
- Ninjurins regulate hematopoietic stem cell amplification through canonical WNT signaling independent of plasma membrane rupture.Nature communications · 2026Article
- Dual activation of NLRP3 and pyrin inflammasomes mediates host responses to the human fungal pathogen Coccidioides.Nature communications · 2026Article
- NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury.Cell death & disease · 2026Article
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
- Translating ferroptosis into oncology: challenges, opportunities and future directions.Nature reviews. Clinical oncology · 2026Review
- Temporal control of Ninj1 activation determines cell-to-cell heterogeneity in IL-33 release.Communications biology · 2026Article
- Cell death pathways and targeting therapeutics in cancer therapy.Acta pharmacologica Sinica · 2026Review
- Research Progress on NINJ1-Mediated Plasma Membrane Rupture Regulation of Pathogen Infection Process.International journal of molecular sciences · 2026Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ferroptosis is a regulated form of necrotic cell death caused by iron-dependent accumulation of oxidized phospholipids in cellular membranes, culminating in plasma membrane rupture (PMR) and cell lysis. PMR is also a hallmark of other types of programmed necrosis, such as pyroptosis and necroptosis, where it is initiated by dedicated pore-forming cell death-executing factors. However, whether ferroptosis-associated PMR is also actively executed by proteins or driven by osmotic pressure remains unknown. Here, we investigate a potential ferroptosis role of ninjurin-1 (NINJ1), a recently identified executor of pyroptosis-associated PMR. We report that NINJ1 oligomerizes during ferroptosis, and that Ninj1-deficiency protects macrophages and fibroblasts from ferroptosis-associated PMR. Mechanistically, we find that NINJ1 is dispensable for the initial steps of ferroptosis, such as lipid peroxidation, channel-mediated calcium influx, and cell swelling. In contrast, NINJ1 is required for early loss of plasma membrane integrity, which precedes complete PMR. Furthermore, NINJ1 mediates the release of cytosolic proteins and danger-associated molecular pattern (DAMP) molecules from ferroptotic cells, suggesting that targeting NINJ1 could be a therapeutic option to reduce ferroptosis-associated inflammation.
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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.