Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis

Atherosclerosis is a multifactorial disease of medium and large arteries, characterized by the presence of lipid-rich plaques lining the intima over time. It is the main cause of cardiovascular diseases and death worldwide. Redox imbalance and lipid peroxidation could play key roles in atheroscleros...

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Main Authors: Anne Nègre-Salvayre, Robert Salvayre
Format: Article
Language:English
Published: MDPI AG 2024-02-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/13/2/232
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author Anne Nègre-Salvayre
Robert Salvayre
author_facet Anne Nègre-Salvayre
Robert Salvayre
author_sort Anne Nègre-Salvayre
collection DOAJ
description Atherosclerosis is a multifactorial disease of medium and large arteries, characterized by the presence of lipid-rich plaques lining the intima over time. It is the main cause of cardiovascular diseases and death worldwide. Redox imbalance and lipid peroxidation could play key roles in atherosclerosis by promoting a bundle of responses, including endothelial activation, inflammation, and foam cell formation. The oxidation of polyunsaturated fatty acids generates various lipid oxidation products such as reactive carbonyl species (RCS), including 4-hydroxy alkenals, malondialdehyde, and acrolein. RCS covalently bind to nucleophilic groups of nucleic acids, phospholipids, and proteins, modifying their structure and activity and leading to their progressive dysfunction. Protein lipoxidation is the non-enzymatic post-translational modification of proteins by RCS. Low-density lipoprotein (LDL) oxidation and apolipoprotein B (apoB) modification by RCS play a major role in foam cell formation. Moreover, oxidized LDLs are a source of RCS, which form adducts on a huge number of proteins, depending on oxidative stress intensity, the nature of targets, and the availability of detoxifying systems. Many systems are affected by lipoxidation, including extracellular matrix components, membranes, cytoplasmic and cytoskeletal proteins, transcription factors, and other components. The mechanisms involved in lipoxidation-induced vascular dysfunction are not fully elucidated. In this review, we focus on protein lipoxidation during atherogenesis.
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spelling doaj.art-0d11bad3d7eb414d9e532bb72f635dcc2024-02-23T15:05:34ZengMDPI AGAntioxidants2076-39212024-02-0113223210.3390/antiox13020232Reactive Carbonyl Species and Protein Lipoxidation in AtherogenesisAnne Nègre-Salvayre0Robert Salvayre1Inserm Unité Mixte de Recherche (UMR), 1297 Toulouse, Centre Hospitalier Universitaire (CHU) Rangueil—BP 84225, 31432 Toulouse CEDEX 4, FranceInserm Unité Mixte de Recherche (UMR), 1297 Toulouse, Centre Hospitalier Universitaire (CHU) Rangueil—BP 84225, 31432 Toulouse CEDEX 4, FranceAtherosclerosis is a multifactorial disease of medium and large arteries, characterized by the presence of lipid-rich plaques lining the intima over time. It is the main cause of cardiovascular diseases and death worldwide. Redox imbalance and lipid peroxidation could play key roles in atherosclerosis by promoting a bundle of responses, including endothelial activation, inflammation, and foam cell formation. The oxidation of polyunsaturated fatty acids generates various lipid oxidation products such as reactive carbonyl species (RCS), including 4-hydroxy alkenals, malondialdehyde, and acrolein. RCS covalently bind to nucleophilic groups of nucleic acids, phospholipids, and proteins, modifying their structure and activity and leading to their progressive dysfunction. Protein lipoxidation is the non-enzymatic post-translational modification of proteins by RCS. Low-density lipoprotein (LDL) oxidation and apolipoprotein B (apoB) modification by RCS play a major role in foam cell formation. Moreover, oxidized LDLs are a source of RCS, which form adducts on a huge number of proteins, depending on oxidative stress intensity, the nature of targets, and the availability of detoxifying systems. Many systems are affected by lipoxidation, including extracellular matrix components, membranes, cytoplasmic and cytoskeletal proteins, transcription factors, and other components. The mechanisms involved in lipoxidation-induced vascular dysfunction are not fully elucidated. In this review, we focus on protein lipoxidation during atherogenesis.https://www.mdpi.com/2076-3921/13/2/232(short chain) RCSlipoxidationoxidative stressprotein adductsinflammationendothelial dysfunction
spellingShingle Anne Nègre-Salvayre
Robert Salvayre
Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
Antioxidants
(short chain) RCS
lipoxidation
oxidative stress
protein adducts
inflammation
endothelial dysfunction
title Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
title_full Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
title_fullStr Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
title_full_unstemmed Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
title_short Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
title_sort reactive carbonyl species and protein lipoxidation in atherogenesis
topic (short chain) RCS
lipoxidation
oxidative stress
protein adducts
inflammation
endothelial dysfunction
url https://www.mdpi.com/2076-3921/13/2/232
work_keys_str_mv AT annenegresalvayre reactivecarbonylspeciesandproteinlipoxidationinatherogenesis
AT robertsalvayre reactivecarbonylspeciesandproteinlipoxidationinatherogenesis