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APE1/Ref-1 redox function prevents VSMC phenotypic switching through KLF4 suppression.

Yeon-Hee Choi1, Eunju Choi2, Sungmin Kim3

  • 1Department of Physiology, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.

Cellular Signalling
|March 6, 2026
PubMed
Summary
This summary is machine-generated.

APE1/Ref-1 deficiency increases oxidative stress, promoting vascular smooth muscle cell (VSMC) switching and neointimal formation. This occurs via redox-dependent KLF4 upregulation, highlighting APE1/Ref-1

Keywords:
APE1/Ref-1Carotid artery ligationKLF4Oxidative stressPhenotypic switchingVascular smooth muscle cell

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Area of Science:

  • Cell Biology
  • Cardiovascular Research
  • Redox Biology

Background:

  • APE1/Ref-1 is a key protein regulating cellular redox homeostasis and gene expression.
  • Vascular smooth muscle cell (VSMC) phenotypic switching is crucial in vascular diseases.
  • Oxidative stress contributes to VSMC dysfunction and pathological vascular remodeling.

Purpose of the Study:

  • To investigate the impact of APE1/Ref-1 deficiency on VSMC phenotypic switching.
  • To elucidate the underlying mechanisms, including the role of oxidative stress and KLF4.
  • To assess the in vivo consequences of APE1/Ref-1 deficiency in vascular remodeling.

Main Methods:

  • Analysis of aorta and VSMCs from heterozygous APE1/Ref-1 deficient mice (APE1/Ref-1+/-).
  • Assessment of oxidative stress markers (ROS, 8-OHdG) and antioxidant enzyme expression.
  • Evaluation of VSMC contractile and proliferative markers (SM22α, α-SMA, PCNA, KLF4).
  • Functional studies involving H₂O₂ treatment, KLF4 knockdown/inhibition, and APE1/Ref-1 overexpression.
  • In vivo assessment of neointimal formation following carotid artery ligation in APE1/Ref-1+/- mice.

Main Results:

  • APE1/Ref-1 deficiency led to increased oxidative stress and reduced antioxidant defenses in VSMCs.
  • APE1/Ref-1+/- VSMCs exhibited reduced contractile markers and increased KLF4 and PCNA expression.
  • Hydrogen peroxide exacerbated VSMC phenotypic switching, while KLF4 modulation reversed these changes.
  • APE1/Ref-1's redox function, not DNA repair, was critical for maintaining contractile phenotype.
  • APE1/Ref-1+/- mice showed increased neointimal hyperplasia after vascular injury.

Conclusions:

  • APE1/Ref-1 deficiency promotes VSMC phenotypic switching and vascular remodeling.
  • Oxidative stress-mediated upregulation of KLF4 is a key mechanism in this process.
  • APE1/Ref-1's redox activity is essential for maintaining vascular homeostasis.