MicroRNAs as Biomarkers of Cardiovascular Diseases

Romakina, V V; Жиров, И. В.; Nasonova, Svetlana N.; Zaseeva, A V; Кочетов, А. Г.; Liang, O V; Tereshchenko, S. N.

doi:10.18087/cardio.2018.1.10083

Cited by 20 publications

(7 citation statements)

References 25 publications

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“…65 Alteration in levels of miRNA have been implicated in conditions such as cervical cancer, ovarian cancer, endometriosis and CVDs. 66–68 Studies have shown differential expression of miRNA in women with PCOS compared with controls, suggesting a potential role of miRNA in PCOS. 69,70 Chen et al have extensively discussed the role of miRNA in PCOS.…”

Section: Origins Of Androgen Excess In Pcos and Pre-receptor Androgenmentioning

confidence: 99%

Implicating androgen excess in propagating metabolic disease in polycystic ovary syndrome

Kempegowda

Melson

Manolopoulos

et al. 2020

Therapeutic Advances in Endocrinology

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Polycystic ovary syndrome (PCOS) has been traditionally perceived as a reproductive disorder due to its most common presentation with menstrual dysfunction and infertility. However, it is now clear that women with PCOS are at increased risk of metabolic dysfunction, from impaired glucose tolerance and type 2 diabetes mellitus to nonalcoholic fatty liver disease and cardiovascular disease. PCOS is characterised by androgen excess, with cross-sectional data showing that hyperandrogenism is directly complicit in the development of metabolic complications. Recent studies have also shown that C11-oxy C19 androgens are emerging to be clinically and biochemically significant in PCOS, thus emphasising the importance of understanding the impact of both classic and C11-oxy C19 androgens on women’s health. Here we discuss androgen metabolism in the context of PCOS, and dissect the role played by androgens in the development of metabolic disease through their effects on metabolic target tissues in women.

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Section: Origins Of Androgen Excess In Pcos and Pre-receptor Androgenmentioning

confidence: 99%

Implicating androgen excess in propagating metabolic disease in polycystic ovary syndrome

Kempegowda

Melson

Manolopoulos

et al. 2020

Therapeutic Advances in Endocrinology

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“…Therefore, finding markers for the early diagnosis of HCC remains the focus of current relevant research. miRNA has become a promising biomolecule for the diagnosis, prognosis, and treatment of tumours with the development of miRNA research [ 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of miRNA-140 on the Growth and Clinical Prognosis of SMMC-7721 Hepatocellular Carcinoma Cell Line

Kong

Chen

Qiu

et al. 2021

BioMed Research International

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Background. A growing number of studies have suggested that microRNAs exert an essential role in the development and occurrence of multiple tumours and act as crucial regulators in various biological processes. However, the expression and function of miRNA-140 in hepatocellular carcinoma (HCC) cells are not yet adequately identified and manifested. Methods. The expression of miRNA-140 was determined in HCC tissues and adjacent nontumour tissues by quantitative real-time polymerase chain reaction (qRT-PCR). Kaplan–Meier survival analysis and Cox regression analysis were performed to explore the correlation between miRNA-140 expression level and the survival rate of patients with HCC. Additionally, overexpression experiments were conducted to investigate the biological role of miRNA-140 in HCC cells. Bioinformatics was used to predict the related target genes and pathways of miRNA-140. Results. QRT-PCR results signified that the expression level of miRNA-140 in HCC was lower than that of adjacent normal tissues ( P < 0.0001 ). Compared with the control group, the SMMC-7721 HCC cells in the miRNA-140 mimic group had a decrease in proliferation, migration, and invasion ( P < 0.05 ), whereas those in the miRNA-140 inhibitor group had an increase in proliferation, migration, and invasion ( P < 0.05 ). Cell cycle arrest occurred in the G0/1 phase. Prognosis analysis showed that the expression level of miRNA-140 was not related to the prognosis of HCC. Furthermore, the Kaplan–Meier test revealed that patients with lower miRNA-140 expression levels in liver cancer tissue had significantly shorter disease-free survival (DFS, P = 0.004 ) and overall survival (OS) times ( P = 0.010 ) after hepatectomy. Cox regression analysis further indicated that miRNA-140 was an independent risk factor that may affect the DFS ( P = 0.004 ) and OS times ( P = 0.014 ) of patients after hepatectomy. Our results suggested that miRNA-140 might be a crucial regulator involved in the HCC progression and is thus considered a potential prognostic biomarker and therapeutic target for HCC.

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“…miRNAs are essential contributors to the modulation of CVD by targeting various genes (23,24). miR-383 is involved in various cellular processes related to the development of various diseases, such as generation of malignancies and cerebral ischemia (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miR-383 suppresses oxidative stress and improves endothelial function by increasing sirtuin 1

Gong

2020

Braz J Med Biol Res

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Previous research has shown that suppression of miR-383 can prevent inflammation of the endothelium, as well as postpone the development of atherosclerosis. However, the role of miR-383 in endothelial cell apoptosis in diabetes remains unclear. The aim of this study was to investigate the function of miR-383 in high glucose-induced apoptosis and oxidative stress in endothelial cells. A series of experiments involving qualitative polymerase chain reaction, cell transfection, luciferase assay, assessment of cell death, detection of catalase and superoxide dismutase concentrations, detection of intracellular reactive oxygen species (ROS), and western blot analysis were performed in this study. We found that miR-383 expression was promoted, while NAD +-dependent deacetylase and sirtuin 1 (SIRT1) expressions were suppressed in the endothelium of the aorta in db/db mice as well as in human umbilical vein endothelial cells, which were treated with high glucose (HG). Increased expression of miR-383 decreased expression of SIRT1, while suppression of miR-383 promoted expression of SIRT1 in human umbilical vein endothelial cells (HUVECs). Furthermore, suppression of miR-383 following transfection with miR-383 suppressor repressed cell death and generation of ROS in HUVECs. SIRT1 knockdown by siRNA-SIRT1 reversed the suppressive effect of miR-383 inhibition on ROS production and cell apoptosis induced by HG treatment. Overall, the findings of our research suggested that suppression of miR-383 repressed oxidative stress and reinforced the activity of endothelial cells by upregulation of SIRT1 in db/db mice, and targeting miR-383 might be promising for effective treatment of diabetes.

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MicroRNAs as Biomarkers of Cardiovascular Diseases

Cited by 20 publications

References 25 publications

Implicating androgen excess in propagating metabolic disease in polycystic ovary syndrome

Implicating androgen excess in propagating metabolic disease in polycystic ovary syndrome

Effects of miRNA-140 on the Growth and Clinical Prognosis of SMMC-7721 Hepatocellular Carcinoma Cell Line

Inhibition of miR-383 suppresses oxidative stress and improves endothelial function by increasing sirtuin 1

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