The role of non-coding RNA network in atherosclerosis

Yuan, Yuchan; Xu, Ling; Geng, Zhaohong; Liu, Jingjing; Zhang, Lijiao; Wu, Yuhang; He, Dan; Qü, Ping

doi:10.1016/j.lfs.2020.118756

Cited by 17 publications

(7 citation statements)

References 142 publications

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“…As an important supplement to traditional genetics, epigenetics contributes to gene modification through DNA methylation/demethylation, histone modification, and non-coding RNA ( Stratton et al, 2019 ; Yuan et al, 2020 ). DNA methylation has been studied in depth due to its stable chemical properties and easy detection.…”

Section: Discussionmentioning

confidence: 99%

“…AS is a complex pathological processes beginning with the accumulation of lipids in damaged vessel walls and oxidative modification to oxidized low-density lipoproteins (ox-LDLs), activation immune system, rapid reaction inflammatory, followed with endothelial cell (ECs) activation, arterial smooth muscle cell (SMC) proliferation, activation of macrophages, and formation of foam cells ( Tabaei and Tabaee, 2019 ). In this process, monocytes/macrophages, vascular smooth muscle cells (VSMCs), and vascular endothelial cells (VECs) are all involved in the pathological process ( Yuan et al, 2020 ; Botts et al, 2021 ). In clinical practice, AS is associated with certain diseases like hyperlipidemia, diabetes mellitus, hyperhomocysteinemia, and hyperuricemia ( Jiang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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DNA Methylation Aberrant in Atherosclerosis

Dai

Chen

2022

Front. Pharmacol.

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Atherosclerosis (AS) is a pathological process involving lipid oxidation, immune system activation, and endothelial dysfunction. The activated immune system could lead to inflammation and oxidative stress. Risk factors like aging and hyperhomocysteinemia also promote the progression of AS. Epigenetic modifications, including DNA methylation, histone modification, and non-coding RNA, are involved in the modulation of genes between the environment and AS formation. DNA methylation is one of the most important epigenetic mechanisms in the pathogenesis of AS. However, the relationship between the progression of AS and DNA methylation is not completely understood. This review will discuss the abnormal changes of DNA methylation in AS, including genome-wide hypermethylation dominating in AS with an increase of age, hypermethylation links with methyl supply and generating hyperhomocysteinemia, and the influence of oxidative stress with the demethylation process by interfering with the hydroxyl-methylation of TET proteins. The review will also summarize the current status of epigenetic treatment, which may provide new direction and potential therapeutic targets for AS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

DNA Methylation Aberrant in Atherosclerosis

Dai

Chen

2022

Front. Pharmacol.

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“…Although the development of atherosclerosis involves a variety of cells [ 36 ], it is mainly initiated by endothelial cell activation through modified lipids such as oxidized low-density lipoprotein [ 37 ]. As a recently recognized type of cellular transdifferentiation, EndMT was first described by Leonard M. Eisenberg in heart development [ 38 ], the concept of which was also put forward to explain the pathophysiological process of atherosclerosis from the perspective of cell transdifferentiation [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

BAG3 Alleviates Atherosclerosis by Inhibiting Endothelial-to-Mesenchymal Transition via Autophagy Activation

Diao

Lan

et al. 2022

Genes

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Atherosclerosis is a chronic systemic inflammatory disease that causes severe cardiovascular events. B cell lymphoma 2-associated athanogene (BAG3) was proven to participate in the regulation of tumor angiogenesis, neurodegenerative diseases, and cardiac diseases, but its role in atherosclerosis remains unclear. Here, we aim to investigate the role of BAG3 in atherosclerosis and elucidate the potential molecular mechanism. In this study, ApoE−/− mice were given a tail-vein injection of BAG3-overexpressing lentivirus and fed a 12-week high-fat diet (HFD) to investigate the role of BAG3 in atherosclerosis. The overexpression of BAG3 reduced plaque areas and improved atherosclerosis in ApoE−/− mice. Our research proves that BAG3 promotes autophagy in vitro, contributing to the suppression of EndMT in human umbilical vein endothelial cells (HUVECs). Mechanically, autophagy activation is mediated by BAG3 via the interaction between BAG3 and its chaperones HSP70 and HSPB8. In conclusion, BAG3 facilitates autophagy activation via the formation of the chaperone-assisted selective autophagy (CASA) complex interacting with HSP70 and HSPB8, leading to the inhibition of EndMT during the progression of atherosclerosis and indicating that BAG3 is a potential therapeutic target for atherosclerosis.

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“…Extracellular ncRNAs are crucial regulators of many cells, including immune cells, macrophages, and endothelial cells. They play a role in atherosclerotic processes such as angiogenesis, foam cell formation, and atherosclerotic plaque progression and rupture [41,54,55]. Extracellular ncRNAs serve as a useful diagnostic indicator and potential treatment target in atherosclerosis [56].…”

Section: Non-coding Rnamentioning

confidence: 99%

Non-Coding RNAs in Regulating Plaque Progression and Remodeling of Extracellular Matrix in Atherosclerosis

Singh

Rai

Agrawal

2022

IJMS

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Non-coding RNAs (ncRNAs) regulate cell proliferation, migration, differentiation, inflammation, metabolism of clinically important biomolecules, and other cellular processes. They do not encode proteins but are involved in the regulatory network of various proteins that are directly related to the pathogenesis of diseases. Little is known about the ncRNA-associated mechanisms of atherosclerosis and related cardiovascular disorders. Remodeling of the extracellular matrix (ECM) is critical in the pathogenesis of atherosclerosis and related disorders; however, its regulatory proteins are the potential subjects to explore with special emphasis on epigenetic regulatory components. The activity of regulatory proteins involved in ECM remodeling is regulated by various ncRNA molecules, as evident from recent research. Thus, it is important to critically evaluate the existing literature to enhance the understanding of nc-RNAs-regulated molecular mechanisms regulating ECM components, remodeling, and progression of atherosclerosis. This is crucial since deregulated ECM remodeling contributes to atherosclerosis. Thus, an in-depth understanding of ncRNA-associated ECM remodeling may identify novel targets for the treatment of atherosclerosis and other cardiovascular diseases.

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The role of non-coding RNA network in atherosclerosis

Cited by 17 publications

References 142 publications

DNA Methylation Aberrant in Atherosclerosis

DNA Methylation Aberrant in Atherosclerosis

BAG3 Alleviates Atherosclerosis by Inhibiting Endothelial-to-Mesenchymal Transition via Autophagy Activation

Non-Coding RNAs in Regulating Plaque Progression and Remodeling of Extracellular Matrix in Atherosclerosis

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