Oxidative Stress: Meeting Multiple Targets in Pathogenesis of Vascular Endothelial Dysfunction.

Curr Drug Targets

School of Pharmaceutical and Population Health Informatics, DIT University, Dehradun-248009, Uttarakhand, India.

Published: August 2022

AI Article Synopsis

  • The vascular endothelium is critical for regulating blood vessel tone, and its dysfunction is linked to various cardiovascular disorders.
  • Numerous factors like over-activation of certain systems and oxidative stress disrupt normal endothelial function, leading to vascular injury and complications.
  • Antioxidants show potential in treating and preventing vascular endothelial dysfunction by countering the harmful effects of oxidative stress.

Article Abstract

The vascular endothelium is the innermost lining of blood vessels, which maintains vasoconstriction and vasodilation. Loss of vascular tone is a hallmark for cardiovascular disorders. Numerous factors, such as over-activation of the renin-angiotensin-aldosterone system, kinases, growth factors, etc., play a crucial role in the induction and progression of vascular abrasion. Interestingly, dysregulation of these pathways either enhances the intensity of oxidative stress, or these pathways are affected by oxidative stress. Thus, oxidative stress has been considered a key culprit in the progression of vascular endothelial dysfunction. Oxidative stress induced by reactive oxygen and nitrogen species causes abnormal gene expression, alteration in signal transduction, and the activation of pathways, leading to induction and progression of vascular injury. In addition, numerous antioxidants have been noted to possess promising therapeutic potential in preventing the development of vascular endothelial dysfunction. Therefore, we have focused on current perspectives in oxidative stress signalling to evaluate common biological processes whereby oxidative stress plays a crucial role in the progression of vascular endothelial dysfunction.

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Source
http://dx.doi.org/10.2174/1389450123666220303090413DOI Listing

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