Report of the National Heart, Lung, and Blood Institute Working Group on Sex Differences Research in Cardiovascular Disease

Maric‐Bilkan, Christine; Arnold, Arthur P.; Taylor, Doris A.; Dwinell, Melinda R.; Howlett, Susan E.; Wenger, Nanette K.; Reckelhoff, Jane F.; Sandberg, Kathryn; Churchill, Gary A.; Levin, Ellis R.; Lundberg, Martha S.

doi:10.1161/hypertensionaha.115.06967

Cited by 61 publications

(41 citation statements)

References 51 publications

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“…This, however, might be explained by the fact that this population-based cohort study examined adolescents, whereas our study focused on the preschool age. It is entirely possible that gender-specific differences also become noticeable in our study population after onset of puberty, as biological sex is considered a major determinant for the development and progression of cardiovascular disease [31]. Longer-term follow-up studies are thus required.…”

Section: Discussionmentioning

confidence: 99%

Former Very Preterm Infants Show an Unfavorable Cardiovascular Risk Profile at a Preschool Age

et al. 2016

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Cardiovascular disease is the leading cause of death worldwide. Evidence points towards an unfavorable cardiovascular risk profile of former preterm infants in adolescence and adulthood. The aim of this study was to determine whether cardiovascular risk predictors are detectable in former very preterm infants at a preschool age. Five- to seven-year-old children born at <32 weeks’ gestational age were included in the study. Same-aged children born at term served as controls. Basic data of study participants were collected by means of follow-up databases and standardized questionnaires. At study visit, anthropometric data, blood pressure readings and aortic intima-media thickness were assessed. Blood samples were obtained after an overnight fast. In comparison to children born at term, former preterm infants had higher systolic and diastolic blood pressure readings (odds ratio [95% confidence interval] per 1-SD higher blood pressure level 3.2 [2.0–5.0], p<0.001 and 1.6 [1.1–1.2], p = 0.008), fasting glucose levels (OR [95% CI] 5.2 [2.7–10.1], p<0.001), homeostasis model assessment index (OR [95% CI] 1.6 [1.0–2.6], p = 0.036), and cholesterol levels (OR [95% CI] 2.1 [1.3–3.4], p = 0.002). Systolic prehypertension (23.7% vs. 2.2%; OR [95% CI] 13.8 [3.1–60.9], p = 0.001), elevated glucose levels (28.6% vs. 5.9%; OR [95% CI] 6.4 [1.4–28.8], p = 0.016), and hypercholesterolemia (77.4% vs. 52.9%; OR [95% CI] 3.0 [1.3–7.1], p = 0.010) were significantly more prevalent in the preterm group. As former very preterm infants display an unfavorable cardiovascular risk profile already at a preschool age, implementation of routine cardiovascular follow-up programs might be warranted.

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Section: Discussionmentioning

confidence: 99%

Former Very Preterm Infants Show an Unfavorable Cardiovascular Risk Profile at a Preschool Age

et al. 2016

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“…In order to account for the potential effects of sex on the observed differences in each phenotype across experimental groups (30), the following variables were included in the model: sex, diet*sex interaction (impact of sex on the diet effect), and genotype*sex interaction (impact of sex on the genotype effect). Differences in the glucose tolerance test profile and body weight over time were evaluated using generalized linear model repeated-measures ANOVA, and a post-hoc Scheffe’s test.…”

Section: Methodsmentioning

confidence: 99%

Characterization of the Cytochrome P450 epoxyeicosanoid pathway in non-alcoholic steatohepatitis

Wells

Vendrov

Edin

et al. 2016

Prostaglandins & Other Lipid Mediators

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Non-alcoholic steatohepatitis (NASH) is an emerging public health problem without effective therapies. Cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid into bioactive epoxyeicosatrienoic acids (EETs), which have potent anti-inflammatory and protective effects. However, the functional relevance of the CYP epoxyeicosanoid metabolism pathway in the pathogenesis of NASH remains poorly understood. Our studies demonstrate that both mice with methionine-choline deficient (MCD) diet-induced NASH and humans with biopsy-confirmed NASH exhibited significantly higher free EET concentrations compared to healthy controls. Targeted disruption of Ephx2 (the gene encoding for soluble epoxide hydrolase) in mice further increased EET levels and significantly attenuated MCD diet-induced hepatic steatosis, inflammation and injury, as well as high fat diet-induced adipose tissue inflammation, systemic glucose intolerance and hepatic steatosis. Collectively, these findings suggest that dysregulation of the CYP epoxyeicosanoid pathway is a key pathological consequence of NASH in vivo, and promoting the anti-inflammatory and protective effects of EETs warrants further investigation as a novel therapeutic strategy for NASH.

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“…1, 2 The overall lifetime risk of cardiovascular disease is similar in the two sexes, but men develop cardiovascular disease earlier than women (Figure 1). 3, 4 At age 55, the lifetime risk of a first incident coronary heart disease is higher in men than women, but the risk of first incident cerebrovascular disease or heart failure is higher in women than men.…”

Section: Introduction: the Importance Of Studying Sex Differences In mentioning

confidence: 99%

Sex Hormones and Sex Chromosomes Cause Sex Differences in the Development of Cardiovascular Diseases

Arnold

Cassis

Eghbali

et al. 2017

ATVB

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245

176

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This review summarizes recent evidence concerning hormonal and sex chromosome effects in obesity, atherosclerosis, aneurysms, ischemia/reperfusion injury, and hypertension. Cardiovascular diseases (CVD) occur and progress differently in the two sexes, because biological factors differing between the sexes have sex-specific protective and harmful effects. By comparing the two 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 CVD, 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 CVDs, 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.

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Report of the National Heart, Lung, and Blood Institute Working Group on Sex Differences Research in Cardiovascular Disease

Cited by 61 publications

References 51 publications

Former Very Preterm Infants Show an Unfavorable Cardiovascular Risk Profile at a Preschool Age

Former Very Preterm Infants Show an Unfavorable Cardiovascular Risk Profile at a Preschool Age

Characterization of the Cytochrome P450 epoxyeicosanoid pathway in non-alcoholic steatohepatitis

Sex Hormones and Sex Chromosomes Cause Sex Differences in the Development of Cardiovascular Diseases

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