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The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: Apr 16, 2026

Portal Vein Injection of Colorectal Cancer Organoids to Study the Liver Metastasis Stroma
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FAP-Activatable Theranostic Agent Inhibiting VEGF Expression for Liver Fibrosis Therapy.

Ni Zeng1, Xiaowen Liu2, Jiayan Peng1

  • 1Department of Cardiology, The Third Affiliated Hospital of Southern Medical University, Southern Medical University, Guangzhou, China.

Advanced Healthcare Materials
|April 15, 2026
PubMed
Summary

A novel nanomedicine, PNPB, targets liver fibrosis (LF) by releasing anti-VEGF drugs when activated by FAP. This theranostic agent shows promise for LF treatment and imaging.

Keywords:
VEGFfibroblast activation proteinliver fibrosisnanomedicinetheranostic agent

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Area of Science:

  • Biomedical Engineering
  • Nanomedicine
  • Hepatology

Background:

  • Liver fibrosis (LF) is a significant fibrotic disorder with limited therapeutic options.
  • Disease progression is linked to angiogenesis driven by vascular endothelial growth factor (VEGF).
  • Effective anti-VEGF therapy for LF and controlled drug release remain clinical challenges.

Purpose of the Study:

  • To develop and evaluate a novel FAP-activatable polymeric nanomedicine (PNPB) for LF theranostics.
  • To assess PNPB's ability to release bevacizumab and a fluorophore upon FAP detection.
  • To investigate PNPB's efficacy in inhibiting VEGF, suppressing angiogenesis, and improving liver function in LF models.

Main Methods:

  • Synthesis of a FAP-activatable polymeric nanomedicine (PNPB) incorporating bevacizumab and a protein-binding fluorophore (PBF).
  • In vitro FAP sensing assay to determine sensitivity.
  • In vivo studies involving LF models to evaluate therapeutic efficacy, liver function, and molecular mechanisms using imaging, western blotting, and immunohistochemistry.

Main Results:

  • PNPB demonstrated high sensitivity in sensing FAP in vitro (0.227 ng/mL).
  • In vivo studies showed PNPB inhibited VEGF expression, suppressed aberrant angiogenesis, alleviated LF, and improved hepatic function.
  • PNPB treatment significantly downregulated key VEGF pathway biomarkers (VEGF, VEGFR1, VEGFR2, Ki67, CD31).

Conclusions:

  • The FAP-activatable nanomedicine PNPB shows significant potential as a theranostic agent for liver fibrosis.
  • The FAP-activatable strategy is a promising approach for designing intelligent nanomedicine for diseases with FAP overexpression.
  • PNPB offers a potential new avenue for LF treatment and imaging, addressing current therapeutic limitations.