Bioelectrical Regulation of Vascular Endothelial Function in Atherosclerosis

Julienne Marie Custodio1, Jianhua J Liu2, Lu Zhang1

  • 1Division of Cardiology, Department of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.

Biomolecules
|July 28, 2026
PubMed

Insights

Ion channels regulate endothelial function, crucial for vascular homeostasis in atherosclerosis. Understanding these bioelectrical signals offers new therapeutic targets for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Vascular Physiology
  • Molecular Medicine

Background:

  • Atherosclerosis is a major cause of cardiovascular death, driven by chronic vascular inflammation and endothelial dysfunction.
  • Endothelial cells utilize bioelectrical signaling via ion channels to maintain vascular homeostasis.
  • Dysregulation of these ion channel pathways contributes to atherosclerotic progression.

Purpose of the Study:

  • To explore the role of ion channels in endothelial function within the context of atherosclerosis.
  • To understand how bioelectrical signaling impacts vascular health and disease.
  • To identify potential therapeutic targets for restoring endothelial homeostasis.

Main Methods:

  • Review of current literature on ion channels and endothelial function in atherosclerosis.
  • Analysis of bioelectrical signaling mechanisms in vascular endothelial cells.
  • Investigation of the link between ion channel dysregulation and atherosclerotic pathology.

Main Results:

  • Ion channels and transporters are central to endothelial bioelectrical signaling.
  • These channels regulate membrane potential, ion flux, calcium, and redox balance.
  • Dysfunctional ion channel activity promotes oxidative stress, inflammation, and endothelial cell death.

Conclusions:

  • Ion channels are critical regulators of endothelial function in atherosclerosis.
  • Targeting ion channel pathways may offer novel therapeutic strategies.
  • Restoring endothelial homeostasis through ion channel modulation can reduce cardiovascular risk.

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