ArticleCellular and molecular life sciences : CMLS2026
IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting USP47 reprograms macrophage polarization to ameliorate septic peritonitis and promote cutaneous wound healing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Mechanism of Action ofBiology · 2026Article
- USP18 Serves as a Key Mediator of cGAS-STING for Cardiac Aging in Diabetes.Cell biochemistry and function · 2026Article
- USP19 alleviates LPS-induced acute lung injury via inhibiting TAK1 activation.Biology direct · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
The imbalance in macrophage M1/M2 polarization is a critical driver of excessive inflammation during the early stage of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), yet its upstream regulatory mechanisms remain incompletely understood. In this study, we investigated the role of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in early ALI pathogenesis. IFIT3 was significantly upregulated in pulmonary macrophages from ALI mice. Functionally, IFIT3 promoted M1 polarization and exacerbated lung inflammatory injury by positively regulating the cGAS-STING pathway. Mechanistically, IFIT3 served as a molecular bridge between STING and the deubiquitinase USP18, thereby inhibiting ubiquitination-mediated degradation of STING and amplifying downstream inflammatory signaling. Furthermore, IFIT3 knockdown ameliorated early lung injury in vivo. In conclusion, our findings demonstrate that IFIT3 promotes macrophage M1 polarization and early inflammation in ALI by scaffolding USP18 to stabilize STING, suggesting its potential as a therapeutic target for ALI/ARDS.
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