ArticleJournal of inflammation research2022
Role of NINJ1 in Gout Flare and Potential as a Drug Target.
Article in Journal of inflammation research, 2022. 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, 11 citations in OpenAlex.
- Metastatic Cancers Exploit Vagal Sensory Neurons and Neural Repair Programs to Colonize New Tissues.Research square · 2026Article
- The role of NINJ1 in diseases.Cell death discovery · 2026Review
- Is Gout an Autoinflammatory Disease?Current rheumatology reports · 2026Review
- Digging deeper into NINJ1: its multifaceted role in central nervous system diseases.Frontiers in immunology · 2026Review
- Gouty arthritis model: delving into disease pathways and uncovering possible therapeutic targets.Frontiers in endocrinology · 2026Review
- Targeting inflammasomes as a therapeutic potential for HIV/AIDS.Cellular and molecular life sciences : CMLS · 2025Review
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- A genome-wide association analysis reveals new pathogenic pathways in gout.Nature genetics · 2024Article
- The pathogenesis of gout: molecular insights from genetic, epigenomic and transcriptomic studies.Nature reviews. Rheumatology · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To determine the role of nerve injury-induced protein 1 (NINJ1) introduced plasma membrane rupture (PMR) and damage-associated molecular patterns (DAMPs) release in the pathogenesis and progression of gout and to explore the potential of NINJ1 as a therapeutic target in gout. Methods: Both peripheral blood mononuclear cells (PBMCs) and serum sample from gout patients (n = 58) and healthy controls (n = 16) were collected and processed to NINJ1 expression, lactate dehydrogenase (LDH) detection, NINJ1 inhibition, and NINJ1 expression experiments, respectively. NINJ1 knockdown was carried out by lentivirus in a monosodium urate (MSU) induced rat model, and NINJ1 neutralizing antibody was applied in a MSU induced mouse model. Results: Our results found that NINJ1 was upregulated during a gout flare, and the resulting induction of PMR correlated with gout progression. NINJ1 knockdown significantly reduced the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and joint swelling in the rat model, and NINJ1 neutralizing antibody also significantly reduced gout flare in the mouse model and PBMCs. Moreover, NINJ1 expression is under NLRP3 inflammasome produced interleukin (IL)-1β control. Conclusion: These results support the notion of a pathogenic role of NINJ1 introduced PMR in gout and provide a detailed mechanism for gout pathogenesis involving inflammatory cell death and DAMPs release introduced by IL-1β. In addition, targeting NINJ1 might be a potential therapeutic approach for gout.
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