Coronary artery disease in women

Sankar, Nainar Madhu; Ramani, Salla Sweta; Anantharaman, R

doi:10.1016/j.ihj.2017.10.008

Cited by 3 publications

(3 citation statements)

References 2 publications

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“…Coronary atherosclerotic heart disease (CHD), also known as coronary heart disease, is caused by coronary atherosclerosis that leads to occlusion and stenosis of the coronary arteries leading to myocardial ischemia and hypoxia in patients ( 1 , 2 ). It is the most common cardiovascular disease for the elderly, and untimely treatment will lead to disability and death, and it is also a kind of disease with high mortality rate in the elderly ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway

et al. 2018

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The present study intended to investigate the effect of fluvastatin on cardiomyocyte apoptosis after myocardial infarction in rats. Eighty myocardial infarction rat models were established and randomly divided into 4 groups (n=20): experimental group (n=20) was given fluvastatin treatment; sham operation group (n=20) and normal control group (n=20) were given saline. The dose of fluvastatin was 20 mg/(kg·d), and irrigation gavage was given for 1 week. Western blot analysis and reverse transcription-quantitative PCR (RT-qPCR) were used to detect the expression of TLR4 mRNA and protein in cardiomyocytes. TUNEL method was used to detect the apoptosis of cardiomyocytes. After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Western blot analysis showed that compared with the myocardial infarction group, the expression of TLR4 protein in normal control group, sham operation group and fluvastatin treatment group were significantly decreased, and they all were statistically significant (P<0.05). TUNEL method found that compared with the myocardial infarction group, the fluvastatin treatment group could significantly reduce the apoptosis of cardiomyocytes (19.2±3.8%), and the difference was statistically significant (P<0.05). Fluvastatin can inhibit myocardial infarction and decrease cardiomyocyte apoptosis by increasing the expression of TLR4-like receptor.

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Section: Introductionmentioning

confidence: 99%

Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway

et al. 2018

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“…As is the leading contributor to Coronary Vascular Disease(CVD), and treatment of atherosclerosis is an essential step towards appropriate management and prevention of CVD 2 . The Burden of disease study in China shows a 20.6% increase in ischemic heart disease mortality from 1990 to 2017 3 . Coronary heart disease is caused by coronary atherosclerosis that leads to occlusion and stenosis of the coronary arteries leading to myocardial ischemia and hypoxia in patients 4 .…”

Section: Introductionmentioning

confidence: 99%

IL-33 / ST2 Signaling Promotes TF Expression by Regulating NF-κB Activation in Coronary Artery Endothelial Microparticles of Acute Myocardial Infarction

Yuan¹,

Cheng²,

Tao³

et al. 2020

Preprint

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Background: Interleukin (IL)-33 was previously shown to induce angiogenesis and inflammatory activation of endothelial cells derived Microparticles（EMPs）. Tissue factor (TF) plays a central role in hemostasis and thrombosis. Objective: The aim of this study was to investigate the effect of IL-33 on TF release of EMPs, which may be a new link between inflammation and coagulation. Methods: The study analyzed the coronary blood of level of CD31+EMPs, TF protein and IL-33 protein in acute myocardial infarction(AMI) and stable coronary artery disease(SCAD) patients. Human coronary artery endothelial cells (HCAECs) were treated with IL-33 to obtain MPs. The TF activity of EMPs was tested by thermo fisher by adding the TF antibody. Furthermore, TF and TFPI protein were tested by ELISA. Finally, NF-κB inhibitor dimethyl fumarate (DMF) and soluble extracellular domain of ST2 coupled to the Fc fragment of human IgG1 (sST2) were added HCAECs, which were treated with IL-33, then the TF protein level also was tested by ELISA. Results: The AMI patients have higher level of CD31+EMPs, TF protein and IL-33 protein than the SCAD patients in coronary blood. In AMI patients (N=27) , the IL-33 protein positively correlated with CD31+EMPs (r = 0.794, p < 0.01). According to the ROC curve analysis, the areas under the curve (AUC) of CD31+EMPs, TF protein and IL-33 protein were 0.888, 0.962 and 0.778. In the cell culture, the TF activity and TF protein in ECs-derived MPs increased gradually with time of intervention by the treatment of IL-33. IL-33 binding to the ST2 receptor promoted TF expression by regulating NF-κB activation in ECs-derived MPs of HCAECs. Conclusion: Activated endothelial cells and their released MPs simultaneously express TF, which is a risk factor for cardiovascular disease.

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“…Cardiovascular disease (CVD) is the most common prevalent types of mortality globally (Sankar, Ramani, & Anantharaman, ). There are various factors that are involved in the pathogenesis of CVD including the formation of atheroma (mainly cholesterol) that accumulates within the artery wall, thrombosis then further narrows the arterial lumen and subsequently reduces the supply of oxygen to the myocardium and other tissues (Alrawi, ).…”

Section: Introductionmentioning

confidence: 99%

Scavenger receptor Class B type I as a potential risk stratification biomarker and therapeutic target in cardiovascular disease

Sahebi

Hassanian

Ghayour‐Mobarhan

et al. 2019

Journal Cellular Physiology

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Cardiovascular disease (CVD) is the leading cause of mortality globally. There are few useful markers available for CVD risk stratification that has proven clinical utility. Scavenger receptor B type I (SR‐BI) is a cell surface protein that plays a major role in cholesterol homeostasis through its interaction with high‐density lipoprotein‐cholesterol (HDL‐C) esters (CE). HDL delivers CE to the liver through selective uptake by the SR‐BI. SR‐BI also regulates the inflammatory response. It has been shown that SR‐BI overexpression has beneficial, protective effects in atherogenesis, and there is considerable interest in developing antiatherogenic strategies that involve SR‐BI‐mediated increases in reverse cholesterol transport through HDL and/or low‐density lipoprotein. Further investigations are essential to explore the clinical utility of this approach. Moreover, there is growing evidence showing associations between genetic variants with modulation of SR‐BI function that may, thereby, increase CVD risk. The aim of the current review was to provide an overview of the possible molecular mechanisms by which SR‐BI may affect CVD risk, and the clinical implications of this, with particular emphasis on preclinical studies on genetic changes of SR‐BI and CVD risk.

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Coronary artery disease in women

Cited by 3 publications

References 2 publications

Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway

Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway

IL-33 / ST2 Signaling Promotes TF Expression by Regulating NF-κB Activation in Coronary Artery Endothelial Microparticles of Acute Myocardial Infarction

Scavenger receptor Class B type I as a potential risk stratification biomarker and therapeutic target in cardiovascular disease

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