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October 12, 2025Frontiers in Bioscience-LandmarkOpen Access

Notch1 Inhibition Exacerbates APAP-Induced Liver Injury via β-Catenin and Macrophage Polarization

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Authors

TYTao YangJDJingjing DaiJZJiangang Zhou

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Overview

Experimental study reveals Notch1 inhibition worsens liver injury during APAP exposure, implicating macrophage polarization and beta-catenin signaling in inflammation.

Key Points

  • Notch1 inhibition significantly exacerbates acetaminophen-induced liver injury, with more severe hepatocellular damage and inflammation.
  • DAPT treatment leads to increased expression of pro-inflammatory cytokines and an M1-like macrophage phenotype.
  • The study identifies the beta-catenin/glycogen synthase kinase 3 beta signaling pathway as a key player in macrophage polarization.
  • These findings point to the Notch1–beta-catenin axis as a crucial regulator in hepatic macrophage function and liver inflammation.

Cite This Study

Yang et al. (2025) studied this question.

synapsesocial.com/papers/68ec1be02b8fa9b2b78ad338https://doi.org/10.31083/fbl43853
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Targeting NOTCH1-KEAP1 axis retards chronic liver injury and liver cancer progression via regulating stabilization of NRF22025
  2. 2Deletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury by reducing accumulation of reparative macrophage and production of HGF2024
  3. 3Notch signaling pathway mediates anti-inflammatory effects of vagus nerve stimulation during lipopolysaccharide-induced acute kidney injury2026
  4. 4Inhibition of Notch signaling pathway attenuates sympathetic hyperinnervation together with the augmentation of M2 macrophages in rats post-myocardial infarction2015 · 75 citations
  5. 5The CXCR2–XBP1–NF-κB Axis Drives Inflammatory Amplification and Tissue Damage in Acute Lung Injury2026