The relationship between fetuin-A and coronary atherosclerotic heart disease (CHD) and CHD-related risk factors: A retrospective study.

ABSTRACT: Fetuin-A plays an important role in antivascular calcification and inflammatory response, it is necessary to explore the relationship between fetuin-A and coronary atherosclerotic heart disease (CHD) and CHD-related risk factors.A total of 92 patients with CHD as the research group, and 60 healthy persons as the control group were enrolled from May 2019 to May 2020. Fetuin-A levels were determined by enzyme-linked immunosorbent assay, and the characteristics and clinical data were collected and compared. Logistic regression was used to analyze the factors influencing CHD.The age, proportion of males, patients with hypertension and diabetes, as well as fetuin-A level in the research group were significantly higher than those in the control group, but the high-density lipoprotein cholesterol level was significantly lower than that in the control group (P < .05). Logistic regression analysis and correction showed that gender, age, blood pressure, and diabetes were related to the onset of CHD, and there was a significant correlation between the level of fetuin-A and age (P < .05).Serum fetuin-A was related to the onset risk of CHD, and showed a significant correlation with age.

The Relationship Between Circulating Neuregulin-1 and Coronary Collateral Circulation in Patients with Coronary Artery Disease.

Coronary collateral circulation (CCC) plays a crucial role in myocardial blood supply, especially for ischemic myocardium. Previous study has shown that neuregulin-1 is a prominent angiogenic factor in diabetic cardiomyopathy, whereas the relationship between neuregulin-1 and CCC has not been investigated. Thus, we aimed to investigate relationship between circulating neuregulin-1 levels and CCC in stable coronary artery disease patients.Coronary artery disease patients with a stenosis of ≥ 90% as evidenced by coronary angiography were included in our study. According to the Rentrop-Cohen classification, coronary collateral degree was graded as 1 to 4. Patients with collateral degree grade 0 or 1 were enrolled in poor CCC group, whereas patients with grade 2 or 3 were enrolled in good CCC group.Plasma neuregulin-1 level was significantly increased in good collateral group and positively related to Rentrop grade (P < 0.01). Multivariate regression analysis and ROC (receiver operating characteristic curve) revealed that plasma neuregulin-1 could predict CCC status effectively.Increased plasma neuregulin-1 level was related to better CCC in patients with coronary artery disease. Neuregulin-1 was an independent and reliable predictor for good coronary collateral development and provided a potential therapeutic strategy to reduce myocardial ischemia injury.

Identification of Differentially Expressed Genes and Signaling Pathways in Acute Myocardial Infarction Based on Integrated Bioinformatics Analysis.

BACKGROUND: Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality around the world. The aim of this research was to determine the differentially expressed genes (DEGs), which may serve as potential therapeutic targets or new biomarkers in AMI. METHODS: From the Gene Expression Omnibus (GEO) database, three gene expression profiles (GSE775, GSE19322, and GSE97494) were downloaded. To identify the DEGs, integrated bioinformatics analysis and robust rank aggregation (RRA) method were applied. These DEGs were performed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses by using Clusterprofiler package. In order to explore the correlation between these DEGs, the interaction network of protein-protein internet (PPI) was constructed using the STRING database. Utilizing the MCODE plug-in of Cytoscape, the module analysis was performed. Utilizing the cytoHubba plug-in, the hub genes were screened out. RESULTS: 57 DEGs in total were identified, including 2 down- and 55 upregulated genes. These DEGs were mainly enriched in cytokine-cytokine receptor interaction, chemokine signaling pathway, TNF signaling pathway, and so on. The module analysis filtered out 18 key genes, including Cxcl5, Arg1, Cxcl1, Spp1, Selp, Ptx3, Tnfaip6, Mmp8, Serpine1, Ptgs2, Il6, Il1r2, Il1b, Ccl3, Ccr1, Hmox1, Cxcl2, and Ccl2. Ccr1 was the most fundamental gene in PPI network. 4 hub genes in total were identified, including Cxcl1, Cxcl2, Cxcl5, and Mmp8. CONCLUSION: This study may provide credible molecular biomarkers in terms of screening, diagnosis, and prognosis for AMI. Meanwhile, it also serves as a basis for exploring new therapeutic target for AMI.

Telmisartan inhibits the proinflammatory effects of homocysteine on human endothelial cells through activation of the peroxisome proliferator-activated receptor-δ pathway.

The aim of this study was to investigate the inhibition capacity of telmisartan to endothelial inflammation induced by homocysteine (Hcy) and discuss the proposed mechanism in vitro. Human umbilical vein endothelial cells (HUVECs) were prepared by collagenase digestion and cultured in vitro. An increase in monocyte chemoattractant protein-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) as markers of Hcy-induced endothelial inflammation. HL-60 cell adhesion to HUVECs was measured by rose bengal staining. Nuclear, cytosolic and total nuclear transcription factor-κB (NF-κB) p65 levels were analyzed by western blotting. Peroxisome proliferator-activated receptor-δ (PPARδ) expression by HUVECs exposed to Hcy with or without telmisartan pretreatment was analyzed by RT-PCR and western blotting. Hcy significantly increased the levels of MCP-1 mRNA, VCAM-1 mRNA and monocyte binding to HUVECs. These effects were significantly attenuated by pretreatment with telmisartan and PPARδ agonists. The effect of telmisartan was inhibited by PPARδ antagonists. The Hcy-mediated downregulation of PPARδ mRNA and protein of HUVECs was inhibited by telmisartan. Hcy-mediated upregulation of NF-κB p65 protein levels in nuclear extracts was inhibited by telmisartan and PPARδ agonists. In conclusion, telmisartan exerts potent anti-inflammatory effects in endothelial cells, probably via a binary mechanism involving PPARδ activation and inhibition of the nuclear translocation of NF-κB.