scholarly journals Cardiac syndrome X. the possible role of Na+-Li+-countertransport activity and other pathophysiological mechanisms in pathogenesis

2013 ◽  
Vol 94 (3) ◽  
pp. 355-361
Author(s):  
V N Oslopov ◽  
Y V Oslopova ◽  
D V Borisov
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vascular Dysfunction ◽  
Syndrome X ◽  
Cardiac Syndrome X ◽  
Pathophysiological Mechanisms ◽  
Cardiac Syndrome ◽  
Number Of Patients

There are numerous pathophysiological mechanisms unequally responsible for the cardiac syndrome X development. The most important is endothelium and smooth muscle cells dysfunction that can intensify vasoconstriction and depress both endothelium-dependant and endothelium-independent vasodilatation, finally leading to coronary micro vascular dysfunction as the basis of the cardiac syndrome X pathogenesis. Together with other possible mechanisms of pathogenesis, studying the importance of increased cell membrane Na+-Li+-countertransport activity seems promising. If was found that a significant number of patients with cardiac syndrome X have increased Na+-Li+-countertransport activity, which is an in vitro marker of Na+-H+-antiporter. Therefore, it is important to measure Na+-Li+-countertransport speed in patients with coronary heart disease, because its high levels increases the chance for cardiac syndrome X, which is a coronary heart disease with no anatomic signs of coronary arteries involvement.

scholarly journals TCTAP A-103 Cardiac Syndrome X – The Role of Endothelial Dysfunction

2016 ◽  
Vol 67 (16) ◽  
pp. S49-S50
Author(s):  
Ashwin Lysander ◽  
Sujai Nikhil Ramakrishnan ◽  
Raghava Chowdary ◽  
Ashish Kansal ◽  
Sri Vidhya
Keyword(s):  
Endothelial Dysfunction ◽  
Syndrome X ◽  
Cardiac Syndrome X ◽  
Cardiac Syndrome

scholarly journals Long Noncoding RNA EZR-AS1 Regulates the Proliferation, Migration, and Apoptosis of Human Venous Endothelial Cells via SMYD3

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Ganhua You ◽  
Xiangshu Long ◽  
Fang Song ◽  
Jing Huang ◽  
Maobo Tian ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Endothelial Cells ◽  
Heart Disease ◽  
Antisense Rna ◽  
Noncoding Rna ◽  
Opposite Effect ◽  
Histone H3 ◽  
Noncoding Rnas

Numerous studies have shown that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of human cardiovascular diseases. However, whether lncRNA ezrin antisense RNA 1 (EZR-AS1) is associated with the progression of coronary heart disease (CHD) remains unclear. Accordingly, the aim of the present study was to evaluate the role of lncRNA EZR-AS1 in patients with CHD and in human venous endothelial cells (HUVECs). The findings revealed that lncRNA EZR-AS1 was highly expressed in the peripheral blood of patients with CHD. In vitro experiments showed that the overexpression of EZR-AS1 could enhance proliferation, migration, and apoptosis by upregulating the expression of EZR in HUVECs; downregulation of lncRNA EZR-AS1 resulted in the opposite effect. lncRNA EZR-AS1 was also found to regulate SET and MYND domain-containing protein 3 (SMYD3), a histone H3 lysine 4-specific methyltransferase, which subsequently mediated EZR transcription. Collectively, these results demonstrate that lncRNA EZR-AS1 plays an important role in HUVECs function via SMYD3 signaling.

scholarly journals Role of adipokine zinc-α2-glycoprotein in coronary heart disease

2019 ◽  
Vol 317 (6) ◽  
pp. E1055-E1062
Author(s):  
Dandan Huang ◽  
Xiaoxiang Mao ◽  
Jiangtong Peng ◽  
Min Cheng ◽  
Tao Bai ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Atherosclerotic Plaques ◽  
293 Cells ◽  
Anti Inflammatory

Zinc-α2-glycoprotein (AZGP1) is a newly identified adipokine that is associated with lipid metabolism and vascular fibrosis. Although adipokines contribute to lipid dysfunction and its related diseases, including stroke and coronary heart disease (CHD), the role of AZGP1 remains unclear. In this study, the role of AZGP1 in atherosclerosis and CHD was investigated. Serum AZGP1 levels from control ( n = 84) and CHD ( n = 91) patients were examined by ELISA and its relationship with various clinical parameters was analyzed. Immunohistochemistry and immunofluorescence were used to detect the expression of AZGP1 and its receptor in coronary atherosclerotic arteries. THP-1 and human embryonic kidney 293 cells were used to verify its anti-inflammatory role in atherosclerosis. Serum AZGP1 levels in CHD patients were lower than controls ( P < 0.01) and independently associated with CHD prevalence ( P = 0.021). AZGP1 levels also inversely correlated with the Gensini score. Immunohistochemistry and immunofluorescence showed that AZGP1 and its receptor β3-adrenoceptor (β3-AR) colocalized in lipid-rich areas of atherosclerotic plaques, particularly around macrophages. In vitro, AZGP1 had no effect on foam cell formation but showed anti-inflammatory effects through its regulation of JNK/AP-1 signaling. In summary, AZGP1 is an anti-inflammatory agent that can be targeted for CHD treatment.

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