Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin, Xiao; Zhan, Jicheng; Wang, Yanjiao; Tan, Pan; Chen, Yiyin; Deng, Hui-Qian; Liu, You‐Shuo

doi:10.1155/2016/6021394

Cited by 47 publications

(46 citation statements)

References 156 publications

(205 reference statements)

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“…Increasing evidence indicate that miRNAs, which are small non-coding RNAs, able to regulate gene expression and to prevent or reduce protein synthesis, have distinct profiles and play crucial roles in various physiological and pathological processes, including vascular aging and inflammation ( 137 – 140 ). An imbalance in the normal miRNA profile can be identified long before the onset of a disease ( 139 , 141 ).…”

Section: Micrornas and Vascular Inflammationmentioning

confidence: 99%

“…Another microRNA, miR-92a, the “atheromiR candidate,” upregulated by oxLDL, is a pro-inflammatory regulator in ECs by modulating inflammatory cytokines and chemokines, enabling monocyte adhesion ( 146 ). MicroRNA-92a controls also neovascularization after ischemic injury ( 140 ). MicroRNAs can also regulate adhesion molecules expression, especially miR-21 and miR-126.…”

Section: Micrornas and Vascular Inflammationmentioning

confidence: 99%

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Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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Arterial stiffness predicts an increased risk of cardiovascular events. Inflammation plays a major role in large arteries stiffening, related to atherosclerosis, arteriosclerosis, endothelial dysfunction, smooth muscle cell migration, vascular calcification, increased activity of metalloproteinases, extracellular matrix degradation, oxidative stress, elastolysis, and degradation of collagen. The present paper reviews main mechanisms explaining the crosstalk between inflammation and arterial stiffness and the most common inflammatory markers associated with increased arterial stiffness, considering the most recent clinical and experimental studies. Diverse studies revealed significant correlations between the severity of arterial stiffness and inflammatory markers, such as white blood cell count, neutrophil/lymphocyte ratio, adhesion molecules, fibrinogen, C-reactive protein, cytokines, microRNAs, and cyclooxygenase-2, in patients with a broad variety of diseases, such as metabolic syndrome, diabetes, coronary heart disease, peripheral arterial disease, malignant and rheumatic disorders, polycystic kidney disease, renal transplant, familial Mediterranean fever, and oral infections, and in women with preeclampsia or after menopause. There is strong evidence that inflammation plays an important and, at least, partly reversible role in the development of arterial stiffness, and inflammatory markers may be useful additional tools in the assessment of the cardiovascular risk in clinical practice. Combined assessment of arterial stiffness and inflammatory markers may improve non-invasive assessment of cardiovascular risk, enabling selection of high-risk patients for prophylactic treatment or more regular medical examination. Development of future destiffening therapies may target pro-inflammatory mechanisms.

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Section: Micrornas and Vascular Inflammationmentioning

confidence: 99%

Section: Micrornas and Vascular Inflammationmentioning

confidence: 99%

Inflammatory Markers for Arterial Stiffness in Cardiovascular Diseases

Malainer²,

et al. 2017

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“…may be partially responsible for cardiovascular disease in such patients. 1,2 Vascular calcification is a ubiquitous phenotype found in the aging population and in diabetes types 1 and 2. 3,4 The mechanisms underlying vascular calcification/aging in diabetes are complex and multifactorial and include high glucose (HG) regulation at the endothelial level.…”

Section: Introductionmentioning

confidence: 99%

LncRNA‐ES3 inhibition by Bhlhe40 is involved in high glucose–induced calcification/senescence of vascular smooth muscle cells

Zhong

Cui

Zhan

et al. 2020

Annals of the New York Academy of Sciences

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Long noncoding RNAs (lncRNAs) have been investigated as novel regulatory molecules involved in diverse biological processes. Our previous study demonstrated that lncRNA‐ES3 is associated with the high glucose–induced calcification/senescence of human aortic vascular smooth muscle cells (HA‐VSMCs). However, the mechanism of lncRNA‐ES3 in vascular calcification/aging remained largely unknown. Here, we report that the expression of basic helix‐loop‐helix family member e40 (Bhlhe40) was decreased significantly in HA‐VSMCs treated with high glucose, whereas the expression of basic leucine zipper transcription factor (BATF) was increased. Overexpression of Bhlhe40 and inhibition of BATF alleviated calcification/senescence of HA‐VSMCs, as confirmed by Alizarin Red S staining and the presence of senescence‐associated β‐galactosidase–positive cells. Moreover, we identified that Bhlhe40 regulates lncRNA‐ES3 in HA‐VSMCs by binding to the promoter region of the lncRNA‐ES3 gene (LINC00458). Upregulation or inhibition of lncRNA‐ES3 expression significantly promoted or reduced calcification/senescence of HA‐VSMCs, respectively. Additionally, we identified that lncRNA‐ES3 functions in this process by suppressing the expression of miR‐95‐5p, miR‐6776‐5p, miR‐3620‐5p, and miR‐4747‐5p. The results demonstrate that lncRNA‐ES3 triggers gene silencing of multiple miRNAs by binding to Bhlhe40, leading to calcification/senescence of VSMCs. Our findings suggest that pharmacological interventions targeting lncRNA‐ES3 may be therapeutically beneficial in ameliorating vascular calcification/aging.

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“…In the present study, we found that high glucose decreases the tel- Vascular aging can change the onset thresholds, process, and severity of a variety of cardiovascular diseases. 2,30 Studies have shown that high glucose is a risk factor for vascular aging in diabetes patients. 4 Senescence of VSMCs has been found to be one of the main contributors of vascular aging.…”

Section: Discussionmentioning

confidence: 99%