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Empagliflozin Attenuates Neointima Formation After Arterial Injury and Inhibits Smooth Muscle Cell Proliferation and

Gwo-Jyh Chang1,2, Wei-Jan Chen2, Yu-Juei Hsu3

  • 1Graduate Institute of Clinical Medicinal Sciences Chang-Gung University College of Medicine Tao-Yuan Taiwan.

Journal of the American Heart Association
|November 7, 2024
PubMed
Abstract

Insights

Empagliflozin inhibits neointima formation by suppressing platelet-derived growth factor (PDGF) signaling, independent of SGLT2. This mechanism offers new insights into preventing vascular stenosis disorders.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Cell Biology

Background:

  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors are known to reduce cardiovascular events.
  • The exact mechanisms underlying these benefits, beyond glycemic control, require further elucidation.
  • Platelet-derived growth factor (PDGF)-related signaling is implicated in vascular remodeling processes.

Purpose of the Study:

  • To investigate the role of PDGF-related signaling in empagliflozin's effects on neointima formation.
  • To determine if empagliflozin's vascular effects are dependent on SGLT2 expression or glycemic control.

Main Methods:

  • Adult male Wistar rats underwent carotid artery balloon injury.
  • Empagliflozin was administered orally before and after injury.
  • In vitro studies assessed empagliflozin's impact on vascular smooth muscle cell (VSMC) proliferation and migration.
  • PDGF signaling pathways (PDGF receptor β, Akt, STAT3 phosphorylation) were analyzed.

Main Results:

  • Empagliflozin significantly reduced neointima formation following balloon injury.
  • Empagliflozin inhibited PDGF-BB-induced VSMC proliferation and migration in vitro.
  • Empagliflozin suppressed PDGF-related signaling pathways.
  • SGLT2 was undetectable in rat VSMCs, and its silencing did not affect empagliflozin's actions.

Conclusions:

  • Empagliflozin's beneficial effects on neointima formation and VSMC function are mediated by suppressing PDGF-related signaling.
  • These vascular protective effects are independent of SGLT2 and glycemic control.
  • This study reveals a novel mechanism for empagliflozin in preventing vascular stenosis.
Keywords:
empagliflozinneointima formationplatelet‐derived growth factorsodium–glucose cotransporter 2vascular smooth muscle cells

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