The research explores the critical role of the pore-forming protein NINJ1 in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). By utilizing single-cell RNA sequencing and experimental models, the authors identify that NINJ1 is upregulated in pro-inflammatory neutrophils and is essential for the release of neutrophil extracellular traps (NETs). This process occurs through NINJ1 oligomerization, which facilitates plasma membrane rupture, allowing the expulsion of large, inflammatory DNA structures. The study demonstrates that genetically deleting Ninj1 in mice significantly reduces lung damage, inflammatory infiltration, and mortality rates. Ultimately, the research highlights NINJ1 as a promising therapeutic target for mitigating the severe pulmonary dysfunction associated with excessive NETosis.
References:
Zhong W J, Liu Y B, Yang X Y, et al. NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury[J]. Cell Death & Disease, 2026.

