scholarly journals Circulating MicroRNA Profiles Differ between Hyperglycemia and Euglycemia in Coronary Heart Disease Patients

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yunyao Jiang ◽  
Nan Liu ◽  
Bingjie Xue ◽  
Jincai Hou ◽  
Chengren Lin ◽  
...  

Coronary heart disease (CHD) has become one of the leading causes of death and functional impairment in the world. Hyperglycemia is associated with an increased risk of cardiovascular disease. It was speculated that miRNAs in peripheral blood were a primary parameter in discriminating CHD. The biological characteristics of coronary heart disease with hyperglycemia (HCHD) and coronary heart disease with euglycemia (ECHD) were investigated in the study. Circulating miRNAs from 26 HCHD patients and 42 ECHD patients were identified by microarrays. Compared with the healthy patients, 15 and 20 differentially expressed miRNAs were identified in HCHD and ECHD groups, respectively. Gene ontology analysis was carried out by DAVID and functional annotations of the miRNA targets related to ATP binding, cellular components, protein binding, RNA binding, DNA binding, and so on. KEGG database was used for pathway analysis. Eleven pathways were identified in both HCHD and ECHD groups. Furthermore, 13 and 3 pathways were only identified in HCHD or ECHD group, respectively. And then, miRNA-gene regulatory networks were constructed to study the relationship between differentially expressed miRNAs and genes. This suggested that hsa-let-7c-5p and hsa-miR-24-3p might have the most important function for hyperglycemia in coronary heart disease patients.

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jincai Hou ◽  
Jun Wang ◽  
Chengren Lin ◽  
Jianhua Fu ◽  
Jianxun Ren ◽  
...  

We compared the circulating microRNA profiles of Qi-stagnation (QSB) and Qi-deficiency (QDB) in coronary heart disease (CHD) patients with blood stasis syndrome. Twenty-nine CHD patients were divided into QSB group and QDB group. The analysis was carried out through comparing their circulating microRNA profiles and the following bioinformatics analysis. The number of differential miRNAs in QDB group was much more than that in QSB group. Functional annotations of the differentially expressed miRNAs target genes in the QSB group and QDB group were, respectively, related to regulation of cellular component organization, regulation of glucose metabolic process, and so forth and protein kinase cascade, phosphate metabolic process, and so forth. KEGG pathway analysis showed that the process Qi-deficiency was associated with phagocytosis including endocytosis and mTOR signaling pathway. Specifically, pathway of cell adhesion molecules played the crucial role in the pathological process of Qi-stagnation, with a unique upregulation except for pathways associated with cancer signal. MicroRNA-gene-net analysis indicated that let-7c, miR-4487, miR-619, miR-8075, miR-6735, and miR-32-5p and miR-17-5p, miR-130a, and miR 320 family had the most important and extensive regulatory function for Qi-stagnation syndromes and Qi-deficiency syndromes, respectively. Differentially expressed miRNAs and concerned pathways suggest different molecular mechanisms that may mediate the pathological process of QSB and QDB syndromes.


2009 ◽  
Vol 21 (9) ◽  
pp. 78
Author(s):  
W. Kong ◽  
R. Nowak ◽  
C. T. Roberts ◽  
J. A. Owens

Placental functional development is characterised by dynamic and co-ordinated changes in expression of genes that drive invasion, differentiation and growth. These changes may arise in part from altered expression of microRNAs (miRNAs) via their regulatory networks. MiRNAs are short, single-stranded, non-coding RNAs involved in the post-transcriptional repression of gene expression. MiRNAs bind to complementary sites in the 3'UTR of target mRNAs to repress or silence translation. MiRNAs have been detected in the mammalian placenta, but their patterns of expression throughout pregnancy have not been systematically characterized. Using microarrays, miRNA gene expression was compared at two stages (6–8 weeks, 10–12 weeks) in early gestation, in chorionic villi of human placentas (term ~40 weeks). Putative and validated targets of differentially expressed miRNAs were extracted from freely accessible databases, miRBase [1], PicTar [2], TargetScan [3] and miRecords [4]. 15 miRNAs were differentially expressed between these gestational ages (p<0.05). 11 of these miRNAs were upregulated in 10–12 week villi and 4 were downregulated. Many of the differentially expressed miRNAs are members of the same polycistronic clusters, suggesting that these miRNAs may be co-expressed. Shared targets of differentially expressed miRNAs from the same clusters were assessed using Ingenuity Pathways Analysis, to search for significantly represented molecular networks. All downregulated miRNAs at 10–12 weeks shared 35 putative targets and fell into 1 of 2 clusters, on chromosome 13 or X. Previously validated targets include PTEN [5], Notch1 [6], VEGFA [7], CDKN2A [8] and DHFR [9] . Six of the upregulated miRNAs at 10–12 weeks are members of 3 clusters on chromosome 19, 9 and X. Networks targeted by these cluster members include PTEN, HIF1α and IL-12 signalling. Together all of these processes are active and important in early placentation and their predicted targeting by differentially expressed miRNAs is consistent with an important role in placental development.


2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


2017 ◽  
Vol 3 ◽  
pp. 233372141769667 ◽  
Author(s):  
Minjee Lee ◽  
M. Mahmud Khan ◽  
Brad Wright

Objective: We investigated the association between childhood socioeconomic status (SES) and coronary heart disease (CHD) in older Americans. Method: We used Health and Retirement Study data from 1992 to 2012 to examine a nationally representative sample of Americans aged ≥50 years ( N = 30,623). We modeled CHD as a function of childhood and adult SES using maternal and paternal educational level as a proxy for childhood SES. Results: Respondents reporting low childhood SES were significantly more likely to have CHD than respondents reporting high childhood SES. Respondents reporting both low childhood and adult SES were 2.34 times more likely to have CHD than respondents reporting both high childhood and adult SES. People with low childhood SES and high adult SES were 1.60 times more likely than people with high childhood SES and high adult SES to report CHD in the fully adjusted model. High childhood SES and low adult SES increased the likelihood of CHD by 13%, compared with high SES both as a child and adult. Conclusion: Childhood SES is significantly associated with increased risk of CHD in later life among older adult Americans.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Elena M. Yubero-Serrano ◽  
Juan F. Alcalá-Diaz ◽  
Francisco M. Gutierrez-Mariscal ◽  
Antonio P. Arenas-de Larriva ◽  
Patricia J. Peña-Orihuela ◽  
...  

Abstract Background Peripheral artery disease (PAD) is recognized as a significant predictor of mortality and adverse cardiovascular outcomes in patients with coronary heart disease (CHD). In fact, coexisting PAD and CHD is strongly associated with a greater coronary event recurrence compared with either one of them alone. High-density lipoprotein (HDL)-mediated cholesterol efflux capacity (CEC) is found to be inversely associated with an increased risk of incident CHD. However, this association is not established in patients with PAD in the context of secondary prevention. In this sense, our main aim was to evaluate the association between CEC and PAD in patients with CHD and whether the concurrent presence of PAD and T2DM influences this association. Methods CHD patients (n = 1002) from the CORDIOPREV study were classified according to the presence or absence of PAD (ankle-brachial index, ABI ≤ 0.9 and ABI > 0.9 and < 1.4, respectively) and T2DM status. CEC was quantified by incubation of cholesterol-loaded THP-1 cells with the participants' apoB-depleted plasma was performed. Results The presence of PAD determined low CEC in non-T2DM and newly-diagnosed T2DM patients. Coexisting PAD and newly-diagnosed T2DM provided and additive effect providing an impaired CEC compared to non-T2DM patients with PAD. In established T2DM patients, the presence of PAD did not determine differences in CEC, compared to those without PAD, which may be restored by glucose-lowering treatment. Conclusions Our findings suggest an inverse relationship between CEC and PAD in CHD patients. These results support the importance of identifying underlying mechanisms of PAD, in the context of secondary prevention, that provide potential therapeutic targets, that is the case of CEC, and establishing strategies to prevent or reduce the high risk of cardiovascular events of these patients. Trial registrationhttps://clinicaltrials.gov/ct2/show/NCT00924937. Unique Identifier: NCT00924937


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Elizabeth J Bell ◽  
Jennifer L St. Sauver ◽  
Veronique L Roger ◽  
Nicholas B Larson ◽  
Hongfang Liu ◽  
...  

Introduction: Proton pump inhibitors (PPIs) are used by an estimated 29 million Americans. PPIs increase the levels of asymmetrical dimethylarginine, a known risk factor for cardiovascular disease (CVD). Data from a select population of patients with CVD suggest that PPI use is associated with an increased risk of stroke, heart failure, and coronary heart disease. The impact of PPI use on incident CVD is largely unknown in the general population. Hypothesis: We hypothesized that PPI users have a higher risk of incident total CVD, coronary heart disease, stroke, and heart failure compared to nonusers. To demonstrate specificity of association, we additionally hypothesized that there is not an association between use of H 2 -blockers - another commonly used class of medications with similar indications as PPIs - and CVD. Methods: We used the Rochester Epidemiology Project’s medical records-linkage system to identify all residents of Olmsted County, MN on our baseline date of January 1, 2004 (N=140217). We excluded persons who did not grant permission for their records to be used for research, were <18 years old, had a history of CVD, had missing data for any variable included in our model, or had evidence of PPI use within the previous year.We followed our final cohort (N=58175) for up to 12 years. The administrative censoring date for CVD was 1/20/2014, for coronary heart disease was 8/3/2016, for stroke was 9/9/2016, and for heart failure was 1/20/2014. Time-varying PPI ever-use was ascertained using 1) natural language processing to capture unstructured text from the electronic health record, and 2) outpatient prescriptions. An incident CVD event was defined as the first occurrence of 1) validated heart failure, 2) validated coronary heart disease, or 3) stroke, defined using diagnostic codes only. As a secondary analysis, we calculated the association between time-varying H 2 -blocker ever-use and CVD among persons not using H 2 -blockers at baseline. Results: After adjustment for age, sex, race, education, hypertension, hyperlipidemia, diabetes, and body-mass-index, PPI use was associated with an approximately 50% higher risk of CVD (hazard ratio [95% CI]: 1.51 [1.37-1.67]; 2187 CVD events), stroke (hazard ratio [95% CI]: 1.49 [1.35-1.65]; 1928 stroke events), and heart failure (hazard ratio [95% CI]: 1.56 [1.23-1.97]; 353 heart failure events) compared to nonusers. Users of PPIs had a 35% greater risk of coronary heart disease than nonusers (95% CI: 1.13-1.61; 626 coronary heart disease events). Use of H 2 -blockers was also associated with a higher risk of CVD (adjusted hazard ratio [95% CI]: 1.23 [1.08-1.41]; 2331 CVD events). Conclusions: PPI use is associated with a higher risk of CVD, coronary heart disease, stroke and heart failure. Use of a drug with no known cardiac toxicity - H 2 -blockers - was also associated with a greater risk of CVD, warranting further study.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Donald Edmondson ◽  
Ian M Kronish ◽  
Jonathan A Shaffer ◽  
Louise Falzon ◽  
Matthew M Burg

Context: Recent evidence suggests that posttraumatic stress disorder (PTSD) may be associated with increased risk for coronary heart disease (CHD). Objective: To determine the association of PTSD to incident CHD using systematic review and meta-analysis. Data Sources: Articles were identified by searching Ovid MEDLINE, PsycINFO, Scopus, Cochrane Library, PILOTS database, and through manual search of reference lists. Study Selection: Prospective cohort studies that assessed PTSD in participants free of CHD and assessed subsequent CHD or cardiac-specific mortality. Data Extraction: We extracted estimates of the association of PTSD to incident CHD, as well as study characteristics. Odds ratios were converted to hazard ratios (HR), and a random-effects model was used to pool results. Data Synthesis: Five studies met our inclusion criteria (N= 401,712); 4 of these included depression as a covariate. The pooled HR for the magnitude of the relationship between PTSD and CHD was 1.53 (95% CI, 1.27-1.84) before adjustment for depression. The pooled HR estimate for the 4 depression-adjusted estimates (N= 362,388) was 1.22 (95% CI, 1.05-1.42). Conclusion: PTSD is independently associated with increased risk for incident CHD, even after adjusting for depression and other covariates. Figure 1. Forest plot of association of PTSD to incident MI or cardiac mortality Note: The area of each square is proportional to the study’s weight in the meta-analysis, and each line represents the confidence interval around the estimate. The diamond represents the aggregate estimate, and its lateral points indicate confidence intervals for this estimate.


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