ArticleInternational journal of biological sciences2025
Targeting NINJ1-Mediated Plasma Membrane Rupture in Tubular Epithelial Cell Prevents Inflammatory Response in Acute Kidney Injury.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- Unveiling the mechanism of metabolites derived from gut microbiota in the treatment of acute kidney injury via network pharmacology and bioinformatics.Bioresources and bioprocessing · 2026Article
- Integrating Bulk and Single-Cell RNA Sequencing Identifies and Validates Lactylation-Related Signatures in Acute Kidney Injury.Biomedicines · 2026Article
- Gastrodin as a nephroprotective agent: Molecular docking-based modulation of oxidative stress, fibrosis, and inflammation.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- PARP7 alleviates lipopolysaccharide-induced acute kidney injury by inhibiting TBK1-driven inflammation in renal tubular epithelial cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- Digging deeper into NINJ1: its multifaceted role in central nervous system diseases.Frontiers in immunology · 2026Review
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage-associated molecular patterns (DAMPs)-induced sterile inflammation is considered as a typical feature of acute kidney injury (AKI). Plasma membrane rupture in renal tubular epithelial cells (RTECs) is the major cause of DAMP release and nerve injury-induced protein 1 (NINJ1) has recently emerged as an executor of plasma membrane rupture, while its role in AKI pathophysiology remains largely unknown. Here, we show upregulated NINJ1 expression and oligomerization in renal tubules among human biopsies and mouse models as well as in cultured RTECs after AKI, accompanied by plasma membrane rupture, increased DAMP release and inflammatory response. Furthermore, knockdown of NINJ1 or inhibition of its oligomerization effectively prevents plasma membrane rupture in RTECs, thereby alleviating DAMP-induced inflammatory response and renal tubular injury. Mechanistically, the ETS transcription factor (ELK1) is identified as a novel transcription factor for NINJ1 during AKI, especially ELK1 phosphorylation at Ser
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