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Pharmacological inhibition of NOX reduces atherosclerotic lesions, vascular ROS and immune-inflammatory responses in

E Di Marco1, S P Gray, P Chew

  • 1Diabetic Complications Division, Baker IDI Heart and Diabetes Institute, PO Box 6429, St Kilda Rd, Melbourne, VIC, 8008, Australia.

Diabetologia
|December 3, 2013
PubMed
Abstract

Insights

Inhibiting NADPH oxidase (NOX)-derived reactive oxygen species (ROS) with GKT137831 reduces inflammation and atherosclerosis in diabetic mice. This study highlights NOX-derived ROS as a key driver of diabetes-accelerated atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Diabetes Complications

Background:

  • Diabetes exacerbates atherosclerosis through vascular inflammation, immune cell infiltration, and reactive oxygen species (ROS) production.
  • NADPH oxidase (NOX)-derived ROS play a significant role in these pro-atherogenic responses.

Purpose of the Study:

  • To investigate the immunomodulatory role of NOX-derived ROS in diabetes-accelerated atherosclerosis.
  • To assess the therapeutic potential of a NOX inhibitor in this context.

Main Methods:

  • Diabetes was induced in Apoe(-/-) mice using streptozotocin.
  • Mice were treated with the NOX inhibitor GKT137831 or vehicle.
  • Atherosclerotic plaque development, immune cell infiltration, ROS production, and inflammatory markers were analyzed.

Main Results:

  • Diabetes significantly increased atherosclerotic plaque area, vascular ROS, and T cell accumulation in aortic sinus and mediastinal lymph nodes.
  • GKT137831 treatment attenuated diabetes-induced atherosclerosis, reduced vascular ROS, and decreased inflammatory markers.
  • NOX inhibition prevented diabetes-mediated increases in plaque size and immune cell infiltration.

Conclusions:

  • Diabetes promotes pro-inflammatory immune responses and NOX-derived ROS production, accelerating atherosclerosis.
  • Blockade of NOX-derived ROS with GKT137831 effectively attenuates these changes.
  • NOX inhibition represents a potential therapeutic strategy for managing diabetes-accelerated atherosclerosis.

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