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New roles for old pathways? A circuitous relationship between reactive oxygen species and cyclo-oxygenase in

Raquel Hernanz1, Ana M Briones, Mercedes Salaices

  • 1*Departamento de Bioquímica, Fisiología y Genética Molecular, Universidad Rey Juan Carlos, Alcorcón, Spain.

Clinical Science (London, England : 1979)
|September 25, 2013
PubMed

Insights

Hypertension involves cyclo-oxygenase (COX) enzymes and reactive oxygen species (ROS). These pathways interact, creating a cycle that worsens vascular dysfunction and hypertension development.

Area of Science:

  • Cardiovascular Research
  • Oxidative Stress Biology
  • Vascular Physiology

Background:

  • Elevated prostanoid production by cyclo-oxygenases (COX-1 and COX-2) is linked to vascular changes in cardiovascular diseases like hypertension.
  • Reactive oxygen species (ROS) significantly contribute to impaired vascular responses and mechanics in hypertension.
  • Cross-talk between NADPH oxidase and mitochondria, key ROS sources in hypertension, forms a feed-forward cycle of ROS production.

Purpose of the Study:

  • To review the current understanding of oxidative stress and COX-derived prostanoids in hypertension-related vascular alterations.
  • To highlight emerging evidence on the synergistic role of ROS and COX pathways in vascular dysfunction.

Main Methods:

  • Literature review of experimental evidence on ROS and COX pathways in hypertension.
  • Analysis of the interplay between ROS and COX-derived products.
  • Discussion of the COX-ROS axis in vascular pathophysiology.

Main Results:

  • ROS can activate COX enzymes, and COX/prostaglandin (PG) synthase pathways can induce ROS production.
  • The COX-ROS axis may form a self-perpetuating cycle of vasoactive products.
  • These pathways act in concert to promote vascular dysfunction in hypertension.

Conclusions:

  • Oxidative stress and COX-derived prostanoids are key contributors to vascular dysfunction in hypertension.
  • The synergistic interaction between COX and ROS pathways represents a critical mechanism in hypertension development.
  • Targeting the COX-ROS axis may offer therapeutic strategies for hypertension.

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