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      Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

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          Abstract

          Objective

          This study aimed to investigate the role of long non‐coding RNA (lncRNA) THRIL in coronary heart disease (CHD) patients.

          Methods

          A total of 420 patients who underwent coronary arteriography due to suspected symptoms of CHD were enrolled, in which 220 were diagnosed as CHD and 200 were set as control subjects. LncRNA THRIL in plasma samples of CHD patients and control subjects was detected by reverse transcription‐quantitative polymerase chain reaction. Gensini score and biochemical indexes were evaluated in CHD patients and control subjects. Plasma inflammatory cytokines were detected, and major adverse cardiovascular events (MACE) were recorded in CHD patients.

          Results

          Both before and after adjustment by age/gender, lncRNA THRIL was increased in CHD patients compared with control subjects (both P < .001), and it well predicted enhanced CHD risk by receiver operating characteristic curves. For coronary artery stenosis, it was positively correlated with Gensini score ( P < .001, r = .430). For clinical characteristics, lncRNA THRIL was positively correlated with diabetes mellitus occurrence ( P < .001) and fasting blood glucose (FBG) level ( P = .029, r = .147). For inflammation, it was positively associated with CRP ( P < .001, r = .374), TNF‐α ( P < .001, r = .249), IL‐1β ( P = .001, r = .222), IL‐8 ( P < .001, r = .254), and IL‐17 ( P = .011, r = .172), while negatively correlated with IL‐10 ( P < .001, r = −.244). For prognosis, lncRNA THRIL was positively associated with MACE accumulating rate ( P = .037) in CHD patients.

          Conclusion

          Long non‐coding RNA THRIL was increased in CHD patients and well predicted elevated CHD risk. Moreover, it was correlated with enhanced coronary stenosis, systematic inflammation, FBG level, and MACE risk in CHD patients.

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          Most cited references15

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          Pathophysiology of coronary artery disease.

          During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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            Effect of Care Guided by Cardiovascular Magnetic Resonance, Myocardial Perfusion Scintigraphy, or NICE Guidelines on Subsequent Unnecessary Angiography Rates: The CE-MARC 2 Randomized Clinical Trial.

            Among patients with suspected coronary heart disease (CHD), rates of invasive angiography are considered too high.
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              • Article: not found

              LncRNAs in vascular biology and disease

              Accumulating studies indicate that long non-coding RNAs (lncRNAs) play important roles in the regulation of diverse biological processes involved in homeostatic control of the vessel wall in health and disease. However, our knowledge of the mechanisms by which lncRNAs control gene expression and cell signaling pathways is still nascent. Furthermore, only a handful of lncRNAs has been functionally evaluated in response to pathophysiological stimuli or in vascular disease states. For example, lncRNAs may regulate endothelial dysfunction by modulating endothelial cell proliferation (e.g. MALAT1, H19) or angiogenesis (e.g. MEG3, MANTIS). LncRNAs have also been implicated in modulating vascular smooth muscle cell (VSMC) phenotypes or vascular remodeling (e.g. ANRIL, SMILR, SENCR, MYOSLID). Finally, emerging studies have implicated lncRNAs in leukocytes activation (e.g. lincRNA-Cox2, linc00305, THRIL), macrophage polarization (e.g. GAS5), and cholesterol metabolism (e.g. LeXis). This review summarizes recent findings on the expression, mechanism, and function of lncRNAs implicated in a range of vascular disease states from mice to human subjects. An improved understanding of lncRNAs in vascular disease may provide new pathophysiological insights and opportunities for the generation of a new class of RNA-based biomarkers and therapeutic targets.
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                Author and article information

                Contributors
                wenchuomi1q7@163.com
                Journal
                J Clin Lab Anal
                J. Clin. Lab. Anal
                10.1002/(ISSN)1098-2825
                JCLA
                Journal of Clinical Laboratory Analysis
                John Wiley and Sons Inc. (Hoboken )
                0887-8013
                1098-2825
                16 January 2020
                May 2020
                : 34
                : 5 ( doiID: 10.1002/jcla.v34.5 )
                : e23196
                Affiliations
                [ 1 ] Department of Cardiology The Central Hospital of Wuhan Tongji Medical College Huazhong University of Science and Technology Wuhan China
                Author notes
                [*] [* ] Correspondence

                Wenping Zhou, Department of Cardiology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, 26 Shengli Street, Wuhan 430014, China

                Emial: wenchuomi1q7@ 123456163.com

                Author information
                https://orcid.org/0000-0001-6765-5878
                Article
                JCLA23196
                10.1002/jcla.23196
                7246374
                31944373
                90d96a1e-e4e4-44ff-a1d4-965791242c07
                © 2020 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 31 October 2019
                : 11 December 2019
                : 18 December 2019
                Page count
                Figures: 4, Tables: 4, Pages: 8, Words: 4803
                Categories
                Research Article
                Research Articles
                Custom metadata
                2.0
                May 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.2 mode:remove_FC converted:25.05.2020

                Clinical chemistry
                coronary heart disease,disease risk,inflammation,long non‐coding rna thril,major adverse cardiovascular events

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