ArticleRedox biology2026
Dual targeting of NCF1 and NLRP3 by roburic acid orchestrates redox homeostasis and inhibits macrophage death in septic lung injury.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated acute lung injury (ALI) is characterized by excessive inflammation and macrophage death, yet precise therapeutic targets remain limited. Single-cell sequencing analysis indicates that, with progression of sepsis-induced lung injury, macrophages exhibit diverse cell-death programs with prominent enrichment of pyroptosis-related signatures. Here, we identify Roburic acid (RBA) as a potent inhibitor of septic ALI and elucidate its mechanism using a nanoparticle delivery system (RBA-NPs). We demonstrate that RBA-NPs significantly attenuate lung injury through a bioactive lipid compound library screening and improve survival in cecal ligation and puncture (CLP)-induced sepsis models. Mechanistically, using chemical proteomics and cellular thermal shift assays, we identify NLRP3 and NCF1 as direct intracellular targets of RBA. Primarily, RBA interacts with the NACHT domain of NLRP3 to directly block inflammasome assembly and pyroptosis. Furthermore, RBA binds to NCF1 to inhibit NADPH oxidase 2 assembly; this restores redox homeostasis, which not only reinforces the suppression of pyroptosis but also confers additional protection by inhibiting lipid peroxidation-mediated ferroptosis. Our study reveals a comprehensive therapeutic strategy where RBA targets the NLRP3 inflammasome while coordinating redox homeostasis via NCF1 to resolve septic lung injury.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.