Non‐coding RNAs in aortic dissection: From biomarkers to therapeutic targets

Cheng, Meng-Die; Yang, Yanyan; Hai, Xin; Li, Min; Zong, Tingyu; He, Xingqiang; Yu, Tao; Hui, Xin

doi:10.1111/jcmm.15802

Cited by 37 publications

(35 citation statements)

References 114 publications

(181 reference statements)

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“…At present, TAD, like aortic aneurysm, has a high mortality rate worldwide. It is still urgent clinically to combine the new adjunctive approach within current interventions (1), and our research demonstrated that Sirt3 activation is expected to be a new target and adjuvant method for the treatment of TAD.…”

Section: Discussionmentioning

confidence: 96%

“…Thoracic aortic dissection (TAD) is the most critical and catastrophic disease of all types of aortic syndrome, which has a rapid onset and a dangerous prognosis (1). When aortic intima has a rupture caused by various reasons, then blood flows into the aortic wall through the rupture, so that the middle layer is peeled from the adventitia to form two cavities.…”

Section: Introductionmentioning

confidence: 99%

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Sirt3 Protects Against Thoracic Aortic Dissection Formation by Reducing Reactive Oxygen Species, Vascular Inflammation, and Apoptosis of Smooth Muscle Cells

Qiu

et al. 2021

Front. Cardiovasc. Med.

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Sirtuin3 (Sirt3) is a histone deacetylase involved in the regulation of many cellular processes. Sirt3 deficiency is known to increase oxidative stress. Reactive oxygen species (ROS) promote degradation of the extracellular matrix and vascular smooth muscle cell (VSMC) apoptosis. Reducing oxidative stress by Sirt3 overexpression could have therapeutic potential for limiting thoracic aortic dissection (TAD) development. We hypothesized that Sirt3 deficiency could increase the risk for TAD by decreasing ROS elimination and that Sirt3 overexpression (Sirt3OE) could provide an alternative option for TAD treatment. Mice with TAD had significantly lower Sirt3 expression than normal subjects. Sirt3 KO mice exhibit significantly increased TAD incidence rate and increased aortic diameters. Moreover, Sirt3 overexpression reduced Ang II-induced ROS production, NF-kB activation, and apoptosis in human aortic smooth muscle cells (HASMCs). Sirt3 overexpression attenuated aneurysm formation and decreased aortic expansion. In conclusion, our data showed that Sirt3 deficiency increases susceptibility to TAD formation by attenuating anti-ROS effects and increasing VSMC apoptosis and vascular inflammation.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Sirt3 Protects Against Thoracic Aortic Dissection Formation by Reducing Reactive Oxygen Species, Vascular Inflammation, and Apoptosis of Smooth Muscle Cells

Qiu

et al. 2021

Front. Cardiovasc. Med.

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“… 37 Recently identified as rising star of the ncRNAs, tsRNAs have been proven to be associated with regulation of RNA processing and protein translation. 38 Additional studies revealed that tRFs and tiRNAs fulfil an important function in multiple diseases. For example, high‐throughput sequencing revealed that tDR‐0009 and tDR‐7336 increased in hypoxia‐treated triple‐negative breast cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Expression profiles and potential roles of transfer RNA‐derived small RNAs in atherosclerosis

Yang

Wang

et al. 2021

J Cellular Molecular Medi

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Atherosclerosis (AS), one of the most common cardiovascular diseases, is the primary cause of morbidity and mortality in the case of cardiac events, thus posing a great threat to human health worldwide. [1][2][3] The disease is characterized by deposition of lipid and other blood components in the intima of the artery, proliferation of smooth muscle cells and increase of collagen fibres, chronic inflammation, plaque formation and hardening of the vascular walls. [3][4][5] The development of atheromatous plaques leads to serious clinical outcomes. 6,7 Once the vulnerable plaques rupture, they induce several clinical conditions, including stroke and myocardial infarction. 8 To date, arteriography is considered to be the gold standard for the diagnosis of AS. However, given the involvement of an invasive procedure, primary injury is

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“…In recent years, the roles of non‐coding RNAs (ncRNAs), including microRNAs, long non‐coding (lnc) RNAs and circulating (circ) RNAs, in disease pathogenesis, regulatory mechanisms and therapeutic applications have gradually become hot areas of research 90‐93 . Moreover, ncRNA has been shown to have an important regulatory role in CVD, 92,94‐105 tumours, 106 inflammation, 103,107 and heart development 108,109 . Increasing studies have shown that ncRNAs constitute potentially important players in biological regulation 110 .…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development

Zhang

Yang

et al. 2021

J Cellular Molecular Medi

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As a common air pollutant, formaldehyde is widely present in nature, industrial production and consumer products. Endogenous formaldehyde is mainly produced through the oxidative deamination of methylamine catalysed by semicarbazide‐sensitive amine oxidase (SSAO) and is ubiquitous in human body fluids, tissues and cells. Vascular endothelial cells and smooth muscle cells are rich in this formaldehyde‐producing enzyme and are easily damaged owing to consequent cytotoxicity. Consistent with this, increasing evidence suggests that the cardiovascular system and stages of heart development are also susceptible to the harmful effects of formaldehyde. Exposure to formaldehyde from different sources can induce heart disease such as arrhythmia, myocardial infarction (MI), heart failure (HF) and atherosclerosis (AS). In particular, long‐term exposure to high concentrations of formaldehyde in pregnant women is more likely to affect embryonic development and cause heart malformations than long‐term exposure to low concentrations of formaldehyde. Specifically, the ability of mouse embryos to effect formaldehyde clearance is far lower than that of the rat embryos, more readily allowing its accumulation. Formaldehyde may also exert toxic effects on heart development by inducing oxidative stress and cardiomyocyte apoptosis. This review focuses on the current progress in understanding the influence and underlying mechanisms of formaldehyde on cardiovascular disease and heart development.

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Non‐coding RNAs in aortic dissection: From biomarkers to therapeutic targets

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 37 publications

References 114 publications

Sirt3 Protects Against Thoracic Aortic Dissection Formation by Reducing Reactive Oxygen Species, Vascular Inflammation, and Apoptosis of Smooth Muscle Cells

Sirt3 Protects Against Thoracic Aortic Dissection Formation by Reducing Reactive Oxygen Species, Vascular Inflammation, and Apoptosis of Smooth Muscle Cells

Expression profiles and potential roles of transfer RNA‐derived small RNAs in atherosclerosis

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development

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