ArticleFrontiers in medicine2026
Downregulation of RORα by alcohol promotes TGFβ and α-SMA expression in mouse lung fibroblasts.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Circadian Rhythms in Acute Respiratory Distress Syndrome: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Circadian regulation of osteoclast lysosomal-resorption machinery: implications for osteoporosis therapy.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Introduction: Chronic ethanol exposure increases susceptibility to fibroproliferative maladaptive repair following acute lung injury. Ethanol disrupts molecular circadian rhythms in multiple organs, contributing to liver steatosis and renal fibrosis. Because circadian disruption is linked to TGFβ activation and tissue fibrosis, we hypothesized that ethanol alters lung circadian signaling and promotes profibrotic responses in lung fibroblasts through modulation of TGFβ and α-SMA expression. Methods: Lung slices from PER2-luciferase reporter mice fed with 20% (v/v) ethanol in drinking water for 8 weeks or only water (control) for 8 weeks were analyzed for real-time bioluminescent PER2 rhythms over 7 days. Lungs from control and ethanol-fed C57BL/6J mice were collected every 4 h over 24 h to assess rhythmicity of selected core clock genes and selected profibrotic markers mRNA expression. Primary murine lung fibroblasts (PLF) were treated with ethanol and evaluated for circadian gene and protein expression. RORα function was interrogated using siRNA knockdown and pharmacological agonist/inverse agonist, followed by analysis of TGFβ, α-SMA, and fibronectin protein levels. Results: Chronic ethanol ingestion lengthened the circadian period by ~2 h ( Conclusion: Ethanol disrupts circadian signaling and enhances profibrotic gene expression in lung fibroblasts, partly through suppression of RORα. RORα activation mitigates these effects, identifying RORα as a potential therapeutic target for ethanol-related maladaptive lung repair.
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