ArticleScientific reports2026
Prostaglandin E2 alleviates acetaminophen-induced liver injury through DDIT4-enhanced autophagy regulated by circLima1/miR-486.
Article in Scientific reports, 2026. 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
Acetaminophen (APAP) overdose is a leading cause of acute liver injury (AILI). While Prostaglandin E2 (PGE2) protects against various forms of acute hepatitis, its underlying mechanisms and the role of circRNA-mediated regulatory networks in AILI remain to be elucidated. AILI was induced in mice by administration of 500 mg/kg APAP, with or without 16,16-dimethyl PGE2 (dmPGE2) pretreatment. Hepatic transcriptomic landscapes (circRNA, miRNA, and mRNA) were characterized by high-throughput sequencing. The circLima1/miR-486/Ddit4 axis was validated using dual-luciferase assays and hepatocyte-specific AAV8-mediated knockdown. Autophagic flux was monitored via mRFP-EGFP-LC3 tandem reporting, and the functional necessity of autophagy was confirmed using the inhibitor 3-methyladenine (3-MA). dmPGE2 treatment reduced serum transaminases and suppressed hepatic p-JNK activation in APAP-challenged mice. Transcriptomic profiling and qPCR identified Ddit4 as a key responder, which was confirmed in primary hepatocytes. Mechanistically, dmPGE2-induced circLima1 sponges miR-486a/b-3p to upregulate DDIT4, leading to inhibited mTOR phosphorylation and enhanced autophagic flux. AAV-mediated knockdown of circLima1 or Ddit4, as well as pharmacological inhibition of autophagy with 3-MA, abolished the hepatoprotective effects of dmPGE2. dmPGE2 alleviates AILI by activating the circLima1/miR-486/DDIT4 axis to promote protective autophagy. These findings identify the circLima1/DDIT4 pathway as a potential therapeutic target for drug-induced liver injury.
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