Coronary heart disease (CHD) is the leading cause of death from cardiovascular disease. This study investigated the expression and clinical significance of long noncoding RNA (lncRNA) autophagy promoting factor (APF) in peripheral blood of patients with acute myocardial infarction (AMI) caused by CHD. Patients with angina pectoris (AP) (n = 80) and AMI (n = 96) and other patients (n = 60) with precordial discomfort but no CHD were included. The serum levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, CDR1AS, miR-188-3p, and cardiac troponin I (cTnI) /creatine kinase (CK) /creatine kinase isozymes (CK-MB) were detected using reverse transcription-quantitative polymerase chain reaction or enzyme-linked immunosorbent assay. Patients with AMI were divided into high/low expression groups based on the median level of APF, and the clinical baseline indicators of patients with AMI were compared. The correlation between lncRNA APF and cTnI/CK/CK-MB/miR-188-3p was analyzed using Pearson analysis, and the clinical value of lncRNA APF was evaluated using the receiver operating characteristic curve. The levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, and CDR1AS in patients with AMI were increased, whereas there were no differences in patients with AP. The APF levels in patients with AMI were higher than MIAT, MALAT1, and CHAST, whereas there were no differences between APF and H19 and CDR1AS. In patients with AMI, the high level of lncRNA APF was correlated with the history of smoking/drinking. Moreover, lncRNA APF was positively correlated with cTnI/CK/CK-MB levels and negatively correlated with miR-188-3p. LncRNA APF has high diagnostic efficacy for AMI. Overall, lncRNA APF is highly expressed in patients with AMI caused by CHD and has high diagnostic efficacy for AMI.
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http://dx.doi.org/10.1536/ihj.21-434 | DOI Listing |
Coronary heart disease (CHD) is the leading cause of death from cardiovascular disease. This study investigated the expression and clinical significance of long noncoding RNA (lncRNA) autophagy promoting factor (APF) in peripheral blood of patients with acute myocardial infarction (AMI) caused by CHD. Patients with angina pectoris (AP) (n = 80) and AMI (n = 96) and other patients (n = 60) with precordial discomfort but no CHD were included.
View Article and Find Full Text PDFBiomed Res Int
April 2022
Guangzhou Xinhua University, 248 Yanjiangxi Road, Machong Town, Dongguan, Guangdong 523133, China.
Atherosclerosis (AS) is a vascular disease with plaque formation. Unstable plaques can be expected to result in cardiovascular disease, such as myocardial infarction and stroke. Studies have verified that long noncoding RNAs (lncRNAs) play a critical role in atherosclerotic plaque formation (APF), including MALAT1, GAS5, and H19.
View Article and Find Full Text PDFCirculation
August 2019
Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York (G.A., A.A.B.).
Background: DNA methylation is implicated in coronary heart disease (CHD), but current evidence is based on small, cross-sectional studies. We examined blood DNA methylation in relation to incident CHD across multiple prospective cohorts.
Methods: Nine population-based cohorts from the United States and Europe profiled epigenome-wide blood leukocyte DNA methylation using the Illumina Infinium 450k microarray, and prospectively ascertained CHD events including coronary insufficiency/unstable angina, recognized myocardial infarction, coronary revascularization, and coronary death.
Biomed Res Int
December 2019
Cardiology Department, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Cardiac remodeling is a self-regulatory response of the myocardium and vasculature under the stressful condition. Cardiomyocytes (CMs), vascular smooth muscle cells (VSMCs), endothelial cells (ECs), and cardiac fibroblasts (CFs) are all involved in this process, characterized by change of morphological structures and mechanical/chemical activities as well as metabolic patterns. Despite current development of consciousness, the control of cardiac remodeling remains unsatisfactory, and to further explore the underlying mechanism and seek the optimal therapeutic targets is still the urgent need in clinical practice.
View Article and Find Full Text PDFCell Physiol Biochem
June 2017
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling.
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