Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis
Atherosclerosis (AS) is a chronic metabolic disorder and primary cause of cardiovascular diseases, resulting in substantial morbidity and mortality worldwide. Initiated by endothelial cell stimulation, AS is characterized by arterial inflammation, lipid deposition, foam cell formation, and plaque de...
Main Author: | |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2023-05-01
|
Series: | International Journal of Molecular Sciences |
Subjects: | |
Online Access: | https://www.mdpi.com/1422-0067/24/11/9338 |
_version_ | 1797597418625171456 |
---|---|
author | Hyunju Kang |
author_facet | Hyunju Kang |
author_sort | Hyunju Kang |
collection | DOAJ |
description | Atherosclerosis (AS) is a chronic metabolic disorder and primary cause of cardiovascular diseases, resulting in substantial morbidity and mortality worldwide. Initiated by endothelial cell stimulation, AS is characterized by arterial inflammation, lipid deposition, foam cell formation, and plaque development. Nutrients such as carotenoids, polyphenols, and vitamins can prevent the atherosclerotic process by modulating inflammation and metabolic disorders through the regulation of gene acetylation states mediated with histone deacetylases (HDACs). Nutrients can regulate AS-related epigenetic states via sirtuins (SIRTs) activation, specifically SIRT1 and SIRT3. Nutrient-driven alterations in the redox state and gene modulation in AS progression are linked to their protein deacetylating, anti-inflammatory, and antioxidant properties. Nutrients can also inhibit advanced oxidation protein product formation, reducing arterial intima-media thickness epigenetically. Nonetheless, knowledge gaps remain when it comes to understanding effective AS prevention through epigenetic regulation by nutrients. This work reviews and confirms the underlying mechanisms by which nutrients prevent arterial inflammation and AS, focusing on the epigenetic pathways that modify histones and non-histone proteins by regulating redox and acetylation states through HDACs such as SIRTs. These findings may serve as a foundation for developing potential therapeutic agents to prevent AS and cardiovascular diseases by employing nutrients based on epigenetic regulation. |
first_indexed | 2024-03-11T03:05:48Z |
format | Article |
id | doaj.art-947584b34e4041e38db21cf30f491895 |
institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-11T03:05:48Z |
publishDate | 2023-05-01 |
publisher | MDPI AG |
record_format | Article |
series | International Journal of Molecular Sciences |
spelling | doaj.art-947584b34e4041e38db21cf30f4918952023-11-18T07:57:39ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-05-012411933810.3390/ijms24119338Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and AtherosclerosisHyunju Kang0Department of Food and Nutrition, Keimyung University, Daegu 42601, Republic of KoreaAtherosclerosis (AS) is a chronic metabolic disorder and primary cause of cardiovascular diseases, resulting in substantial morbidity and mortality worldwide. Initiated by endothelial cell stimulation, AS is characterized by arterial inflammation, lipid deposition, foam cell formation, and plaque development. Nutrients such as carotenoids, polyphenols, and vitamins can prevent the atherosclerotic process by modulating inflammation and metabolic disorders through the regulation of gene acetylation states mediated with histone deacetylases (HDACs). Nutrients can regulate AS-related epigenetic states via sirtuins (SIRTs) activation, specifically SIRT1 and SIRT3. Nutrient-driven alterations in the redox state and gene modulation in AS progression are linked to their protein deacetylating, anti-inflammatory, and antioxidant properties. Nutrients can also inhibit advanced oxidation protein product formation, reducing arterial intima-media thickness epigenetically. Nonetheless, knowledge gaps remain when it comes to understanding effective AS prevention through epigenetic regulation by nutrients. This work reviews and confirms the underlying mechanisms by which nutrients prevent arterial inflammation and AS, focusing on the epigenetic pathways that modify histones and non-histone proteins by regulating redox and acetylation states through HDACs such as SIRTs. These findings may serve as a foundation for developing potential therapeutic agents to prevent AS and cardiovascular diseases by employing nutrients based on epigenetic regulation.https://www.mdpi.com/1422-0067/24/11/9338nutrientsacetylation statevascular inflammationatherosclerosis |
spellingShingle | Hyunju Kang Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis International Journal of Molecular Sciences nutrients acetylation state vascular inflammation atherosclerosis |
title | Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis |
title_full | Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis |
title_fullStr | Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis |
title_full_unstemmed | Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis |
title_short | Regulation of Acetylation States by Nutrients in the Inhibition of Vascular Inflammation and Atherosclerosis |
title_sort | regulation of acetylation states by nutrients in the inhibition of vascular inflammation and atherosclerosis |
topic | nutrients acetylation state vascular inflammation atherosclerosis |
url | https://www.mdpi.com/1422-0067/24/11/9338 |
work_keys_str_mv | AT hyunjukang regulationofacetylationstatesbynutrientsintheinhibitionofvascularinflammationandatherosclerosis |