ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage-to-Myofibroblast Transition in Chronic Pancreatitis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A review of the sirtuins family: pivotal regulators and emerging therapeutic targets in renal fibrosis.Renal failure · 2026Review
- SIRT7-mediated ACSL3 delactylation suppresses colorectal cancer progression by orchestrating tumor-associated macrophage ferroptosis and polarization.Cell death & disease · 2026Article
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- Identification of a Novel PDRG1-EZH2-p21 Pathway Controlling Senescence and Tumor Progression in Hepatocellular Carcinoma.International journal of biological sciences · 2026Article
- UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage-to-Myofibroblast Transition in Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
10 authors.
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Abstract
Chronic pancreatitis (CP) is a progressive inflammatory disease characterized by pancreatic fibrosis and functional decline. Here, we identify macrophage-to-myofibroblast transition (MMT) as a novel feature of CP and investigate the role of mitochondrial uncoupling protein 2 (UCP2) in this process. Using mouse models, human pancreatic specimens, and cell lines, we show that UCP2 is markedly upregulated in CP, primarily in acinar cells. UCP2 knockout reduces MMT and alleviates fibrosis, whereas macrophage depletion reverses this protective effect, confirming the central role of MMT. Metabolomic profiling reveals that UCP2 knockout alters lipid metabolism by downregulating acyl-CoA synthetase long-chain family member 3 (ACSL3) and reducing lipid droplet (LD) release in acinar cells. Mechanistically, UCP2 upregulation increases silent information regulator 1 (Sirt1) expression, enhances Smad3 phosphorylation and nuclear translocation, and activates transforming growth factor-β (TGF-β)/Smad3 signaling to promote macrophage MMT. Macrophage-specific Sirt1 knockout suppresses both fibrosis and MMT. In conclusion, UCP2 drives CP progression by regulating ACSL3-mediated LD release in acinar cells and modulating macrophage function through the Sirt1/Smad3 pathway. Targeting UCP2 may represent a promising therapeutic strategy for CP.
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Registered trials
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