Increased serum galectin-3 level is associated with endothelial dysfunction and cardiovascular events in patients

Hui-Sheng Wang1, Bang-Gee Hsu2, Ji-Hung Wang1,3,4

  • 1Division of Cardiology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.

Heliyon
|January 6, 2025
PubMed

Insights

Higher galectin-3 (Gal-3) levels are linked to poor vascular reactivity and increased cardiovascular events in hypertension patients. This suggests Gal-3 may play a role in hypertension-induced endothelial dysfunction.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Inflammation Research

Background:

  • Endothelial dysfunction is a precursor to cardiovascular complications.
  • Galectin-3 (Gal-3) is implicated in inflammatory cardiac diseases.
  • The specific role of Gal-3 in hypertension-related endothelial dysfunction requires clarification.

Purpose of the Study:

  • To investigate the association between serum galectin-3 (Gal-3) levels and endothelial dysfunction in hypertensive patients.
  • To evaluate the relationship between Gal-3 levels and long-term cardiovascular outcomes in this cohort.

Main Methods:

  • 120 hypertensive patients were enrolled, with 7-year cardiovascular outcome monitoring.
  • Serum Gal-3 levels were quantified using enzyme-linked immunosorbent assay.
  • Vascular reactivity index (VRI) was assessed via digital thermal monitoring.

Main Results:

  • Poor vascular reactivity was observed in 12 patients, intermediate in 57, and good in 51.
  • Factors associated with poor endothelial dysfunction included older age, elevated cholesterol and LDL, lower eGFR, and higher Gal-3 levels.
  • Higher Gal-3 levels correlated with lower VRI and were linked to increased cardiovascular events over 7 years.

Conclusions:

  • Elevated serum Gal-3 levels are associated with endothelial dysfunction in hypertensive individuals.
  • Higher Gal-3 levels predict adverse cardiovascular events in patients with hypertension.
  • Galectin-3 may be a significant factor in the pathophysiology of hypertension-induced endothelial dysfunction.
Abstract

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