MicroRNA-23b prevents aortic aneurysm formation by inhibiting smooth muscle cell phenotypic switching via FoxO4 suppression

Si, Xiaoyan; Chen, Qixian; Zhang, Jiechang; Zhou, Wei; Chen, Lijun; Chen, Jingjing; Deng, Na; Li, Wei; Liu, Danan; Wang, Long; Shi, Linyan; Sun, Weihong; Song, Hui‐Hua; Zhong, Lintao

doi:10.1016/j.lfs.2021.119092

Cited by 11 publications

(9 citation statements)

References 48 publications

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“…A considerable number of studies are being conducted to better understand the pathogenesis of AA and to find innovative and feasible means of prevention and treatment. Previous studies have suggested that VSMCs apoptosis is a critical part of atherogenesis, but according to recent studies, the VSMCs phenotype is altered before or early during the establishment of aneurysms [ 68 ]. Ailawadi and his team found that VSMCs contraction markers were downregulated and matrix metalloproteinases were upregulated early in aneurysmogenesis, suggesting that VSMCs phenotypic transformation occurs during this period.…”

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

“…MiR-23b expression was observed by Si et al to be considerably reduced in the aorta of angiotensin II-treated ApoE −/− mice. In an in vitro test, knocking down miRNA-23b during an angiotensin II-induced VSMCs phenotypic transition greatly boosted the expression of the transcription factor Forkhead box O4 (FoxO4), which stabilizes the VSMCs contractile phenotype and protects against AAA formation [ 68 ].…”

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

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Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

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Vascular smooth muscle cells (VSMCs), the major cell type in the arterial vessel wall, have a contractile phenotype that maintains the normal vessel structure and function under physiological conditions. In response to stress or vascular injury, contractile VSMCs can switch to a less differentiated state (synthetic phenotype) to acquire the proliferative, migratory, and synthetic capabilities for tissue reparation. Imbalances in VSMCs phenotypic switching can result in a variety of cardiovascular diseases, including atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification. It is very important to identify the molecular mechanisms regulating VSMCs phenotypic switching to prevent and treat cardiovascular diseases with high morbidity and mortality. However, the key molecular mechanisms and signaling pathways participating in VSMCs phenotypic switching have still not been fully elucidated despite long-term efforts by cardiovascular researchers. In this review, we provide an updated summary of the recent studies and systematic knowledge of VSMCs phenotypic switching in atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification, which may help guide future research and provide novel insights into the prevention and treatment of related diseases.

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Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

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“…The elucidation of the molecular mechanisms regulating the pathological conditions responsible for the development of diseases could provide valuable information that could be useful in developing new methods for the management of these diseases. Many recent studies have shown that miRNAs are promising targets for the diagnosis and treatment of various conditions, including LEAD [ 49 , 50 , 51 , 52 , 53 , 54 ], AAA [ 28 , 55 , 56 , 57 ], and CVD [ 58 , 59 ]. In particular, many investigations were carried out to evaluate the utility of proangiogenic properties of miRNAs in the therapy of peripheral atherosclerosis [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

miRNA Regulatory Networks Associated with Peripheral Vascular Diseases

Zalewski

Ruszel

Stępniewski

et al. 2022

JCM

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A growing body of evidence indicates a crucial role of miRNA regulatory function in a variety of mechanisms that contribute to the development of diseases. In our previous work, alterations in miRNA expression levels and targeted genes were shown in peripheral blood mononuclear cells (PBMCs) from patients with lower extremity artery disease (LEAD), abdominal aortic aneurysm (AAA), and chronic venous disease (CVD) in comparison with healthy controls. In this paper, previously obtained miRNA expression profiles were compared between the LEAD, AAA, and CVD groups to find either similarities or differences within the studied diseases. Differentially expressed miRNAs were identified using the DESeq2 method implemented in the R programming software. Pairwise comparisons (LEAD vs. AAA, LEAD vs. CVD, and AAA vs. CVD) were performed and revealed 10, 8, and 17 differentially expressed miRNA transcripts, respectively. The functional analysis of the obtained miRNAs was conducted using the miRNet 2.0 online tool and disclosed associations with inflammation and cellular differentiation, motility, and death. The miRNet 2.0 tool was also used to identify regulatory interactions between dysregulated miRNAs and target genes in patients with LEAD, AAA, and CVD. The presented research provides new information about similarities and differences in the miRNA-dependent regulatory mechanisms involved in the pathogenesis of LEAD, AAA, and CVD.

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“…In another study, miRNA-23b overexpression in ApoE −/− mice infused with Ang II prevented AAA formation in this model [ 63 ]. Further, maintenance of the mature vSMC contractile phenotype was promoted by miRNA-23b, which targets and negatively regulates FoxO4 [ 64 ]. Further, in separate studies, miRNA-23b was shown to inhibit phenotypic modulation and neointimal hyperplasia in a carotid model of restenosis post balloon angioplasty [ 65 ].…”

Section: Epigenetic Modifications In Smooth Muscle Cells and Fibrobla...mentioning

confidence: 99%

The Role of Epigenetic Modifications in Abdominal Aortic Aneurysm Pathogenesis

2022

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Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high morbidity and mortality in the setting of acute rupture. Recently, advances in surgical and endovascular repair of AAA have been achieved; however, pharmaceutical therapies to prevent AAA expansion and rupture remain lacking. This highlights an ongoing need to improve the understanding the pathological mechanisms that initiate formation, maintain growth, and promote rupture of AAA. Over the past decade, epigenetic modifications, such as DNA methylation, posttranslational histone modifications, and non-coding RNA, have emerged as important regulators of cellular function. Accumulating studies reveal the importance of epigenetic enzymes in the dynamic regulation of key signaling pathways that alter cellular phenotypes and have emerged as major intracellular players in a wide range of biological processes. In this review, we discuss the roles and implications of epigenetic modifications in AAA animal models and their relevance to human AAA pathology.

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MicroRNA-23b prevents aortic aneurysm formation by inhibiting smooth muscle cell phenotypic switching via FoxO4 suppression

Cited by 11 publications

References 48 publications

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

miRNA Regulatory Networks Associated with Peripheral Vascular Diseases

The Role of Epigenetic Modifications in Abdominal Aortic Aneurysm Pathogenesis

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