scholarly journals Sex differences in hypertension and other cardiovascular diseases

2018 ◽  
Vol 36 (4) ◽  
pp. 768-770 ◽  
Author(s):  
Christian Delles ◽  
Gemma Currie
2021 ◽  
Vol 2 ◽  
Author(s):  
Cinthya Echem ◽  
Eliana H. Akamine

Human life span expectancy has increased, and aging affects the organism in several ways, leading, for example, to an increased risk of cardiovascular diseases. Age-adjusted prevalence of the cardiovascular diseases is higher in males than females. Aging also affects the gonadal sex hormones and the sex differences observed in cardiovascular diseases may be therefore impacted. Hormonal changes associated with aging may also affect the immune system and the immune response is sexually different. The immune system plays a role in the pathogenesis of cardiovascular diseases. In this context, toll-like receptors (TLRs) are a family of pattern recognition receptors of the immune system whose activation induces the synthesis of pro-inflammatory molecules. They are expressed throughout the cardiovascular system and their activation has been widely described in cardiovascular diseases. Some recent evidence demonstrates that there are sex differences associated with TLR responses and that these receptors may be affected by sex hormones and their receptors, suggesting that TLRs may contribute to the sex differences observed in cardiovascular diseases. Recent evidence also shows that sex differences of TLRs in cardiovascular system persists with aging, which may represent a new paradigm about the mechanisms that contribute to the sex differences in cardiovascular aging. Therefore, in this mini review we describe the latest findings regarding the sex differences of TLRs and associated signaling in cardiovascular diseases during aging.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Ana Queirós ◽  
Claudia Eschen ◽  
Daniela Fliegner ◽  
Vera Regitz-Zagrosek ◽  
Hugo Sanchez Ruderisch

Sex differences (SD) in cardiovascular diseases are described and have been attributed to the effects of sex hormones, such as estrogen (E2). Our previous studies in a mouse model of pressure overload revealed SD in fibrosis and apoptosis related genes that were abolished in estrogen receptor β deficient (ERβ-/-) mice. Other studies focus on miRNA regulation by E2, but little is known about sex-specific regulation of miRNAs in heart diseases. We hypothesize that E2 and ERβ are regulators of miRNA expression in the heart potentially contributing to the molecular mechanism of SD observed in cardiovascular diseases. This project aims to identify SD in the expression of miRNAs in a 9-week transverse aortic constriction (TAC) model and the possible role of E2 and ERβ in their regulation in the heart. A Targetscan analysis of 80 sex-specific dysregulated genes in hypertrophy allowed identifying 157 different miRNAs that could target them. Based on their expression in the heart we selected 60 miRNAs for quantification by qRT-PCR. In WT mice, 23 miRNAs showed SD in their expression in hypertrophy, all of them showing a higher expression in males than in females. All these significant SD were abolished in ERβ-/- mice. A direct comparison of some of these miRNAs in WT and ERβ-/- female animals identified nine miRNAs significantly higher expressed in the knock-out animals (let-7e, miR-106b, miR-130a, miR-133a, miR-20a, miR-24, miR-27b, miR-29a and miR-378). In vitro studies performed using a female cardiomyocyte cell line (AC16) showed a down-regulation of eight of these miRNAs after a 48h treatment with E2, being the exception miR-133a. The latter showed however a down-regulation after 48h treatment with an ERβ specific agonist, as well as let-7e, miR-106b, miR-130a, miR-20a, miR-24, miR-27b and miR-29a. The effect of treatment with ERα was only visible as a down-regulation of miR-24, miR-29a and miR-378. The potential of these miRNAs having targets in the same pathway and acting in a synergistic way is still under investigation. ERβ is for the first time identified as a major regulator of miRNA expression in the heart. It may play an important role in determining SD in cardiac hypertrophy, being responsible for the inhibition of miRNA expression in the female heart.


Author(s):  
Yuichi Jono ◽  
Takashi Kohno ◽  
Shun Kohsaka ◽  
Hiroki Kitakata ◽  
Yasuyuki Shiraishi ◽  
...  

2012 ◽  
Vol 30 (12) ◽  
pp. 2378-2386 ◽  
Author(s):  
Maria Lorenza Muiesan ◽  
Ettore Ambrosioni ◽  
Francesco Vittorio Costa ◽  
Gastone Leonetti ◽  
Achille Cesare Pessina ◽  
...  

2017 ◽  
Vol 37 (5) ◽  
pp. 746-756 ◽  
Author(s):  
Arthur P. Arnold ◽  
Lisa A. Cassis ◽  
Mansoureh Eghbali ◽  
Karen Reue ◽  
Kathryn Sandberg

This review summarizes recent evidence concerning hormonal and sex chromosome effects in obesity, atherosclerosis, aneurysms, ischemia/reperfusion injury, and hypertension. Cardiovascular diseases occur and progress differently in the 2 sexes, because biological factors differing between the sexes have sex-specific protective and harmful effects. By comparing the 2 sexes directly, and breaking down sex into its component parts, one can discover sex-biasing protective mechanisms that might be targeted in the clinic. Gonadal hormones, especially estrogens and androgens, have long been found to account for some sex differences in cardiovascular diseases, and molecular mechanisms mediating these effects have recently been elucidated. More recently, the inherent sexual inequalities in effects of sex chromosome genes have also been implicated as contributors in animal models of cardiovascular diseases, especially a deleterious effect of the second X chromosome found in females but not in males. Hormonal and sex chromosome mechanisms interact in the sex-specific control of certain diseases, sometimes by opposing the action of the other.


2021 ◽  
Author(s):  
Valery V. Gafarov ◽  
Dmitriy O. Panov ◽  
Elena A. Gromova ◽  
Igor V. Gagulin ◽  
Almira V. Gafarova ◽  
...  

Introduction: The study aimed to determine gender differences in the prevalence and dynamics of affective states over a long period, i.e., 23 years, and to establish their effect on the risk of cardiovascular diseases (CVD), i.e., arterial hypertension (AH), myocardial infarction (MI), and stroke among the population aged 25–64 in Russia / Siberia. Methods: Between 1994 and 2017, we conducted 4 screening surveys of representative samples (totalling 4,815 people) under the international programs MONICA and HAPIEE in Russia / Siberia. To determine the sex differences in cardiovascular risk from 1994 to 2010, we observed cohorts formed from the screened individuals without CVD and diabetes mellitus (DM). Results: High levels of affective states in the period from 1994 to 2003, especially in women, were replaced by a downward trend in 2013. At the same time, there was a reduction in the gender gap in terms of frequency of depression lower 1%, and men in the younger age groups reported higher levels of personal anxiety (49.3% vs 46.1% in adults aged 35-44y) and vital exhaustion (16.9% vs 15.6%) than women in 2017. We found that men with unfavourable levels of affective states have a 3–5 fold higher risk of hypertension and stroke, while women have a higher risk of myocardial infarction (p for all < 0.05). Hostility in men is associated with a negative risk of myocardial infarction and stroke (HR=0.3 and HR=0.29, respectively; p for all < 0.05). However, this was levelled out by unfavourable social characteristics. Conclusions: The downward trends in prevalence of psychosocial factors were unstable and associated with reduced gender gap for affective states. It had a significant impact on the gender magnitude of cardiovascular risk.


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