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Azilsartan ameliorates ox-LDL-induced endothelial dysfunction via promoting the expression of KLF2

Wenfeng Li1,2, Chenggao Wang2, Dandan Zhang2

  • 1Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou 510630, Guangdong, China.

Aging
|May 4, 2021
PubMed

Insights

Azilsartan protects against oxidized LDL-induced endothelial dysfunction by increasing Krüppel-like factor 2 (KLF2) expression. This mechanism helps restore nitric oxide production and reduce inflammation in cardiovascular disease models.

Area of Science:

  • Cardiovascular Research
  • Endothelial Biology
  • Pharmacology

Background:

  • Oxidized LDL (ox-LDL) contributes to cardiovascular diseases like atherosclerosis by causing endothelial dysfunction.
  • Azilsartan, an angiotensin II receptor blocker, is used to treat hypertension.
  • The potential protective effects of Azilsartan against ox-LDL-induced endothelial damage and its mechanism require investigation.

Purpose of the Study:

  • To investigate Azilsartan's efficacy in ameliorating ox-LDL-induced endothelial cell dysfunction.
  • To explore the underlying molecular mechanisms, focusing on Krüppel-like factor 2 (KLF2).

Main Methods:

  • An in vitro endothelial dysfunction model was created using human umbilical vascular endothelial cells (HUVECs) exposed to ox-LDL.
  • Gene and protein expression (LOX-1, eNOS, occludin, KLF2) and mediator production (MCP-1, CXCL1, NO) were analyzed.
  • Endothelial permeability and the role of KLF2 were assessed using FITC-dextran assays and KLF2 silencing.

Main Results:

  • Azilsartan significantly suppressed ox-LDL-induced increases in LOX-1, MCP-1, and CXCL-1.
  • It reversed ox-LDL-induced downregulation of eNOS and nitric oxide (NO) production.
  • Azilsartan treatment improved endothelial barrier function and occludin expression, effects dependent on KLF2, and increased KLF2 expression inhibited by ox-LDL.

Conclusions:

  • Azilsartan demonstrates a protective effect against ox-LDL-induced endothelial damage.
  • The mechanism involves the upregulation of KLF2, which subsequently improves endothelial function and barrier integrity.
Abstract

Keywords:
Azilsartanatherosclerosisendothelial dysfunctionox-LDL

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