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Nrf2 and Heme Oxygenase-1 Involvement in Atherosclerosis Related Oxidative Stress

Journal

ANTIOXIDANTS
Volume 10, Issue 9, Pages -

Publisher

MDPI
DOI: 10.3390/antiox10091463

Keywords

atherosclerosis; oxidative stress; heme oxygenase-1; Nrf2

Funding

  1. Institute of Health Carlos III, ISCIII [PI16-00784 PI17/00130, PI20/00375, PI20-00716]
  2. Spanish Ministry of Science and Innovation [RYC-2017-22369]
  3. Spanish Society of Nephrology (SEN), Consejeria de Salud y Familias-FEDER, Junta de Andalucia [PIGE-0052-2020]
  4. Programa Operativo de Andalucia-FEDER, Iniciativa Territorial Integrada ITI 2014-2020, Consejeria de Salud, Junta de Andalucia [PI0026-2017]
  5. European Regional Development Fund. A way to make Europe
  6. Spanish Biomedical Research Center in Cardiovascular Diseases (CIBERCV)

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Atherosclerosis, the underlying cause of cardiovascular diseases and high mortality rates, progresses with the formation of atherosclerotic plaques due to oxidative stress. Strategies aimed at reducing oxidative damage, including the use of antioxidant molecules such as Nrf2 and HO-1, have been studied to inhibit the progression of atherosclerosis.
Atherosclerosis remains the underlying process responsible for cardiovascular diseases and the high mortality rates associated. This chronic inflammatory disease progresses with the formation of occlusive atherosclerotic plaques over the inner walls of vascular vessels, with oxidative stress being an important element of this pathology. Oxidation of low-density lipoproteins (ox-LDL) induces endothelial dysfunction, foam cell activation, and inflammatory response, resulting in the formation of fatty streaks in the atherosclerotic wall. With this in mind, different approaches aim to reduce oxidative damage as a strategy to tackle the progression of atherosclerosis. Special attention has been paid in recent years to the transcription factor Nrf2 and its downstream-regulated protein heme oxygenase-1 (HO-1), both known to provide protection against atherosclerotic injury. In the current review, we summarize the involvement of oxidative stress in atherosclerosis, focusing on the role that these antioxidant molecules exert, as well as the potential therapeutic strategies applied to enhance their antioxidant and antiatherogenic properties.

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