ArticleJournal of inflammation research2025
STK11 Alleviates Pulmonary Inflammation During Acute Lung Injury by Phosphorylating AMPK to Activate Autophagy in A549 Cell Model.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: To investigate if protein STK11 alleviates lipopolysaccharide-induced acute lung injury (ALI), hypothesizing it activates autophagy (harmful substance clearance) via AMPK's "start signal". Methods: Researchers used a genomics-first approach: they integrated datasets GSE66890, GSE10474, and GSE32707, screened autophagy-related differentially expressed genes in ALI via bioinformatics, and confirmed STK11 as a key regulator through protein-protein interaction analysis. They treated human lung cells with 50 μg/mL lipopolysaccharide for 24 hours to establish ALI models, then overexpressed or silenced STK11 in the cells. They assessed cell function, apoptosis, inflammatory factors, autophagy activity, and AMPK activation. Results: Researchers verified STK11 as a key regulator of autophagy in ALI. STK11 overexpression significantly improved cell function, reduced apoptosis (lower pro-apoptotic/higher anti-apoptotic proteins), decreased IL-6/IL-8/TNF-α (mRNA/protein levels), enhanced autophagy (elevated LC3B-II, reduced P62, more autophagosomes), and activated AMPK. STK11 silencing reversed these protective effects and inhibited AMPK. Conclusion: STK11 mitigates lipopolysaccharide-induced lung cell damage by activating AMPK-mediated autophagy, emerging as a potential therapeutic target for ALI.
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