The impact of early menopause on risk of coronary artery disease (PREmature Coronary Artery Disease In Women – PRECADIW case-control study)

Lubiszewska, Barbara; Kruk, Mariusz; Broda, Grażyna; Księżycka, Ewa; Piotrowski, Walerian; Kurjata, Paweł; Zieliński, Tomasz; Płoski, Rafał

doi:10.1177/1741826710394269

Cited by 37 publications

(16 citation statements)

References 21 publications

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“…It should be noted that all female CAD subjects in this study are postmenopausal. It has been long-known that, due to the loss of the protective effects by hormone, CAD risk increased in postmenopausal women [34][35][36] . Interestingly, one recent report suggested that reduction of circulating nitric oxide (NO) may account for the decrease in the number and dysfunction of ECFCs in postmenopausal hypercholesterolemic women 37 .…”

Section: Discussionmentioning

confidence: 99%

miR-548aq-3p is a novel target of Far infrared radiation which predicts coronary artery disease endothelial colony forming cell responsiveness

Tsai

Chiang²,

et al. 2020

Sci Rep

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Non-invasive far infrared radiation (FIR) has been observed to improve the health of patients with coronary artery disease (CAD). Endothelial colony forming cells (ECFCs) contribute to vascular repair and CAD. The goal of this study was to uncover the role of FIR in ECFCs function and to reveal potential biomarkers for indication of FIR therapy in CAD patients. FIR significantly enhanced in vitro migration (transwell assay) and tube formation (tube length) capacities in a subpopulation of CAD ECFCs. Clinical parameters associated with the responsiveness of ECFCs to FIR include smoking and gender. ECFCs from CAD patients that smoke did not respond to FIR in most cases. In contrast, ECFCs from females showed a higher responsiveness to FIR than ECFCs from males. To decipher the molecular mechanisms by which FIR modulates ECFCs functions, regardless of sex, RNA sequencing analysis was performed in both genders of FIR-responsive and FIR-non/unresponsive ECFCs. Gene Ontology (GO) analysis of FIR up-regulated genes indicated that the pathways enriched in FIR-responsive ECFCs were involved in cell viability, angiogenesis and transcription. Small RNA sequencing illustrated 18 and 14 miRNAs that are up-and down-regulated, respectively, in FIR-responsive CAD ECFCs in both genders. Among the top 5 up-and down-regulated miRNAs, down-regulation of miR-548aq-3p in CAD ECFCs after FIR treatment was observed in FIR-responsive CAD ECFCs by RT-qPCR. Down-regulation of miR-548aq-3p was correlated with the tube formation activity of CAD ECFCs enhanced by FIR. After establishment of the down-regulation of miR-548aq-3p by FIR in CAD ECFCs, we demonstrated through overexpression and knockdown experiments that miR-548aq-3p contributes to the inhibition of the tube formation of ECFCs. This study suggests the down-regulation of miR-548aq-3p by FIR may contribute to the improvement of ECFCs function, and represents a novel biomarker for therapeutic usage of FIR in CAD patients.open Scientific RepoRtS | (2020) 10:6805 | https://doi.org/10.1038/s41598-020-63311-1 www.nature.com/scientificreports www.nature.com/scientificreports/ progenitor cells (EPCs). The classification of EPC has been applied to multiple cell types, including endothelial colony forming cells (ECFCs) 2 . ECFCs exhibit the ability to form colonies after prolonged culture and proliferate after re-plating in an in vitro culture system. These cells are identified as positive for VE-cadherin, VEGFR2 (vascular endothelial growth factor receptor 2), VEGFR1, CD31, CD105, CD146, VWF (von Willebrand factor), CD34, and negative for CD14, CD45, CD115, CD133 3 . ECFCs have the potential to incorporate into the endothelial layer and differentiate into mature ECs, thereby contributing to repair of injured vascular endothelium as well as forming new blood vessels 4 . ECFCs can further enhance vasculogenic properties by releasing trophic factors 5 . With these capacities, ECFCs have been suggested to function in maintaining vascular homeostasis and preventing CAD. In line with this, increas...

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Section: Discussionmentioning

confidence: 99%

miR-548aq-3p is a novel target of Far infrared radiation which predicts coronary artery disease endothelial colony forming cell responsiveness

Tsai

Chiang²,

et al. 2020

Sci Rep

View full text Add to dashboard Cite

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“…It is well established that early onset menopause increases the risk for cardiovascular disease (40). While the mechanisms involved are not yet known, testosterone is indicated as a potential mediator (41).…”

Section: Discussionmentioning

confidence: 99%

Chronic Blockade of the Androgen Receptor Abolishes Age-Dependent Increases in Blood Pressure in Female Growth-Restricted Rats

et al. 2016

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Intrauterine growth restriction induced via placental insufficiency programs a significant increase in blood pressure at 12 months of age in female growth-restricted rats that is associated with early cessation of estrous cyclicity indicative of premature reproductive senescence. In addition, female growth-restricted rats at 12 months of age exhibit a significant increase in circulating testosterone with no change in circulating estradiol. Testosterone is positively associated with blood pressure after menopause in women. Thus, we tested the hypothesis that androgen receptor blockade would abolish the significant increase in blood pressure that develops with age in female growth-restricted rats. Mean arterial pressure was measured in animals pretreated with and without the androgen receptor antagonist, flutamide (8 mg/kg/day, sc for 2 weeks). Flutamide abolished the significant increase in blood pressure in growth-restricted rats relative to control at 12 months of age. To examine the mechanism(s) by which androgens contribute to increased blood pressure in growth-restricted rats, blood pressure was assessed in rats untreated or treated with enalapril (250 mg/L for 2 weeks). Enalapril eliminated the increase in blood pressure in growth-restricted relative to vehicle- and flutamide-treated controls. Furthermore, the increase in medullary angiotensin type 1 receptor mRNA expression was abolished in flutamide-treated growth-restricted relative to untreated counterparts and controls; cortical angiotensin converting enzyme mRNA expression was reduced in flutamide-treated growth-restricted versus untreated counterparts. Thus, these data indicate that androgens, via activation of the renin angiotensin system, are important mediators of increased blood pressure that develops by 12 months of age in female growth-restricted rats.

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“…17 Additionally, there are several nontraditional cardiac risks unique to or predominant in women, including early menopause or menarche, gestational diabetes mellitus, hypertension, preeclampsia and eclampsia during pregnancy, and systemic inflammatory disorders (Figure 2). [18][19][20][21] The 2013 American College of Cardiology/American Heart Association (AHA) guidelines on assessment of CVD risk recommend the use of ASCVD risk calculator, which accounts for sex and ethnic diversity but not the emerging risk factors prevalent in women. 22 …”

Section: Risk Factorsmentioning

confidence: 99%

Sex Differences in Ischemic Heart Disease

Aggarwal

Patel

Mehta

et al. 2018

Circ: Cardiovascular Quality and Outcomes

211

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Evolving knowledge of sex-specific presentations, improved recognition of conventional and novel risk factors, and expanded understanding of the sex-specific pathophysiology of ischemic heart disease have resulted in improved clinical outcomes in women. Yet, ischemic heart disease continues to be the leading cause of morbidity and mortality in women in the United States. The important publication by the Institute of Medicine titled "Women's Health Research-Progress, Pitfalls, and Promise," highlights the persistent disparities in cardiovascular disease burden among subgroups of women, particularly women who are socially disadvantaged because of race, ethnicity, income level, and educational attainment. These important health disparities reflect underrepresentation of women in research, with the resultant unfavorable impact on diagnosis, prevention, and treatment strategies in women at risk for cardiovascular disease. Causes of disparities are multifactorial and related to differences in risk factor prevalence, access to care, use of evidence-based guidelines, and social and environmental factors. Lack of awareness in both the public and medical community, as well as existing knowledge gap regarding sex-specific differences in presentation, risk factors, pathophysiology, and response to treatment for ischemic heart disease, further contribute to outcome disparities. There is a critical need for implementation of sex-and gender-specific strategies to improve cardiovascular outcomes. This review is tailored to meet the needs of a busy clinician and summarizes the contemporary trends, characterizes current sex-specific outcome disparities, delineates challenges, and proposes transformative solutions for improvement of the full spectrum of ischemic heart disease clinical care and research in women.by guest on May 7, 2018

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The impact of early menopause on risk of coronary artery disease (PREmature Coronary Artery Disease In Women – PRECADIW case-control study)

Abstract: We have shown that smoking and early postmenopausal stage (≤3 years) are the most important determinants of premature CAD followed by parental CVD, diabetes and hypertension.

Cited by 37 publications

References 21 publications

miR-548aq-3p is a novel target of Far infrared radiation which predicts coronary artery disease endothelial colony forming cell responsiveness

miR-548aq-3p is a novel target of Far infrared radiation which predicts coronary artery disease endothelial colony forming cell responsiveness

Chronic Blockade of the Androgen Receptor Abolishes Age-Dependent Increases in Blood Pressure in Female Growth-Restricted Rats

Sex Differences in Ischemic Heart Disease

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