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  • Research Article   
  • Atheroscler Open Access 9: 252.,
  • DOI: 10.4172/asoa.1000252

The Role of the Renin-Angiotensin Axis, Oxidised Low-Density Lipoproteins, Insulin Resistance, Dyslipidaemia, and Hyperglycaemia in Endothelial Impairment: Implications for Vasodilation and Autoimmunity

Patrono Enrico Salvatore*
Department of Cardiovascular Disease, University of Montreal, Italy
*Corresponding Author : Patrono Enrico Salvatore, Department of Cardiovascular Disease, University of Montreal, Italy, Email: patrono1279@gmail.com

Received Date: May 01, 2024 / Published Date: May 30, 2024

Abstract

Endothelial impairment, characterized by dysfunction in the inner lining of blood vessels, is a hallmark of various cardiovascular diseases. This research article explores the multifaceted role of several key factors in the pathogenesis of endothelial dysfunction. Specifically, we investigate the involvement of the renin-angiotensin axis, oxidised lowdensity lipoproteins, insulin resistance, dyslipidaemia, and hyperglycaemia in compromising endothelial integrity. Moreover, we examine how increased expression of pro-inflammatory cytokines and adhesion molecules contributes to vasodilatory dysfunction in the endothelium. Additionally, we discuss the influence of autoimmunity on exacerbating endothelial dysfunction. By elucidating these mechanisms, this study provides insights into potential therapeutic targets for mitigating endothelial impairment and preventing associated cardiovascular complications.

Citation: Salvatore PE (2024) The Role of the Renin-Angiotensin Axis, Oxidised Low-Density Lipoproteins, Insulin Resistance, Dyslipidaemia, and Hyperglycaemia in Endothelial Impairment: Implications for Vasodilation and Autoimmunity. Atheroscler Open Access 9: 252. Doi: 10.4172/asoa.1000252

Copyright: © 2024 Salvatore PE. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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