Circulating Noncoding RNAs as Biomarkers of Cardiovascular Disease and Injury

Viereck, Janika; Thum, Thomas

doi:10.1161/circresaha.116.308434

Cited by 329 publications

(282 citation statements)

References 144 publications

(226 reference statements)

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“…Serum and plasma miRNAs are probably the most suitable source for clinical application as sample collection is quick, simple, and reproducible. Indeed, miRNAs are remarkably stable and resistant in the blood and long-term storage or freezing/thawing cycles do not seem to cause problems (28, 29). Interestingly, circulating miRNAs are protected from endogenous high levels of RNase activity in the blood since they are linked to carriers in vesicles or non-vesicular forms (30).…”

Section: Micrornasmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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Over the last decades, life expectancy has significantly increased although several chronic diseases persist in the population, with aging as the leading risk factor. Despite improvements in diagnosis and treatment, many elderlies suffer from cardiovascular problems that are much more frequent in an older, more fragile organism. In the long term, age-related cardiovascular diseases (CVDs) contribute to the decline of quality of life and ability to perform normal activities of daily living. microRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the posttranscriptional level in both physiological and pathological conditions. In this review, we will focus on the role of miRNAs in aging and age-related CVDs as heart failure, hypertension, atherosclerosis, atrial fibrillation, and diabetes mellitus. miRNAs are key regulators of complex biological mechanisms, representing an exciting potential therapeutic target in CVDs. Moreover, one major challenge in geriatric medicine is to find reliable biomarkers for diagnosis, prognosis, and prediction of the response to specific drugs. miRNAs represent a very promising tool due to their stability in the circulation and unique signature in CVDs. However, further studies are needed to investigate their translational potential in the real clinical practice.

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Section: Micrornasmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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“…Previous studies have shown that lncRNA can be used as a competitive endogenous RNA (ceRNA) and interacts with miRNAs, participates in the regulation of expression of target genes, and plays an important role in the progression of cardiovascular disease [6]. Zhou et al demonstrated XIST promoted myocardial infraction by targeting miR-130a-3p [7].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA XR007793 Regulates Proliferation and Migration of Vascular Smooth Muscle Cell via Suppressing miR-23b

Zhang

Cui

et al. 2018

Med Sci Monit

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BackgroundLong noncoding RNAs (lncRNAs) were identified as potential regulatory factor in vascular disease. However, the role of XR007793 in the regulation of neointima formation after vascular injury remains largely unknown.Material/MethodsLncRNA expression levels were detected using real-time polymerase chain reaction (RT-PCR). In vivo and in vitro assay were performed in Sprague-Dawley rats and VSMCs. Cell Counting Kit-8 (CCK-8) assay, Transwell assay, and scratch wound healing assay were performed to detect cell proliferation and migration. Western blotting was used to detect protein expression.ResultsThe results of qRT-PCR indicated that XR007793 expression was significantly increased in the injured carotid artery of Sprague-Dawley rats and platelet-derived growth factor-BB induced rat aortic smooth muscle cells. Knockdown of XR007793 repressed the proliferation and migration of VSMC in vitro. The expression level of miR-23b was reduced in mouse carotid injured tissues and cell line. Bioinformatics analysis and luciferase reporter assay revealed that XR007793 directly bonds to miR-23b. Pearson correlation analysis showed that XR007793a and miR-23b were negatively correlated in carotid samples. Furthermore, bioinformatics analysis and luciferase assay indicated that miR-23b targeted the Forkhead box O 4 (FOXO4) 3′-UTR to inhibit FOXO4 expression. After transfecting miR-23b inhibitor, the expression both of XR007793 and FOXO4 was increased. The effects on expression were reversed after transfected with miR-23b mimics. Rescue experiments results indicated that miR-23b inhibitor reduced the expression of VSMC marker and promoted proliferation and migration of VSMC.ConclusionsThis study shows that XR007793 aggravates the loss of function of VSMCs by negatively regulating miR-23b. It does so by targeting FOXO4, which could serve as a novel therapeutic target in post-angioplasty restenosis.

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“…The Pitx2c gene, expressed in the left compartment of the heart at embryonic stage, and in the left atrium, pulmonary vein, and right ventricle after birth, can inhibit Shox2 expression through direct interaction with its promoter (Ai et al 2006;Nowotschin et al 2006;Wang et al 2010Wang et al , 2014Ammirabile et al 2012) and indirectly regulates Shox2 expression through the inhibitory effects of microRNAs (miR-1792 and miR-106b-25) (Viereck and Thum 2017). The latter phenomenon is due to the expression of Pitx2c in the left heart compartment; thus, the Shox2 expression is restricted in SAN tissue of the right atrium, and the SAN differentiation and development are activated via Shox2-inhibited Nkx2.5 expression.…”

Section: Fig 2 Schematic Representation Of Shox2 and Shox2 Proteinsmentioning

confidence: 99%

Shox2: The Role in Differentiation and Development of Cardiac Conduction System

Xin

Zhao

et al. 2018

Tohoku J. Exp. Med.

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The formation and conduction of electrocardiosignals and the synchronous contraction of atria and ventricles with rhythmicity are both triggered and regulated by the cardiac conduction system (CCS). Defect of this system will lead to various types of cardiac arrhythmias. In recent years, the research progress of molecular genetics and developmental biology revealed a clearer understanding of differentiation and development of the cardiac conduction system and their regulatory mechanisms. Short stature homeobox 2 (Shox2) transcription factor, encoded by Shox2 gene in the mouse, is crucial in the formation and differentiation of the sinoatrial node (SAN). Shox2 drives embryonic development processes and is widely expressed in the appendicular skeleton, palate, temporomandibular joints, and heart. Mutations of Shox2 can lead to dysembryoplasia and abnormal phenotypes, including bradycardiac arrhythmia. In this review, we provide a summary of the latest research progress on the regulatory effects of the Shox2 gene in differentiation and development processes of the cardiac conduction system, hoping to deepen the knowledge and understanding of this systematic process based on the cardiac conduction system. Overall, the Shox2 gene is intimately involved in the differentiation and development of cardiac conduction system, especially sinoatrial node. We also summarize the current information about human SHOX2. This review article provides a new direction in biological pacemaker therapies.

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Circulating Noncoding RNAs as Biomarkers of Cardiovascular Disease and Injury

Cited by 329 publications

References 144 publications

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Long Noncoding RNA XR007793 Regulates Proliferation and Migration of Vascular Smooth Muscle Cell via Suppressing miR-23b

Shox2: The Role in Differentiation and Development of Cardiac Conduction System

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