Endogenous Sex Hormones and Cardiovascular Disease in Men

Muller, Majon; Schouw, Yvonne T. van der; Thijssen, J. H. H.; Grobbee, Diederick E.

doi:10.1210/jc.2003-030611

Cited by 118 publications

(74 citation statements)

References 143 publications

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“…However, the mechanism underlying sex differences in cardiovascular risk is poorly understood. Although deleterious effects of androgens and beneficial effects of ovarian hormones have been proposed, recent studies suggest that male hormones have a neutral or beneficial effect on the heart (Muller et al 2003). A previous study of Npr1K/K mice proposed a role for testosterone in aggravating the hypertrophy in young, male mice (Li et al 2004), in which the castration of Npr1 KO male mice reduced cardiac hypertrophy and fibrosis, whereas Figure 4 The contractile function at different levels of left ventricular end-diastolic pressure (LVEDP) in WT (C/C), heterozygous (K/C) and KO (K/K) Npr1 male mice at 8 weeks and 6 months of age.…”

Section: Discussionmentioning

confidence: 99%

Npr1-regulated gene pathways contributing to cardiac hypertrophy and fibrosis

Ellmers¹,

Scott

Piuhola

et al. 2007

Journal of Molecular Endocrinology

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The natriuretic peptides, atrial (ANP) and brain natriuretic peptide (BNP) are known to suppress cardiac hypertrophy and fibrosis. Both ANP and BNP exert their bioactivities through the Npr1 receptor, and Npr1 knockout mice (Npr1K/K) exhibit marked cardiac hypertrophy and fibrosis. In this study, we investigated which genes within the hypertrophic and fibrotic pathways are influenced by the lack of Npr1 signalling. cDNA microarray and quantitative real-time PCR (RT-PCR) analyses were performed on cardiac ventricles from Npr1K/K mice. Gene expression at early and late stages during development of hypertrophy was investigated in male and female Npr1K/K mice at 8 weeks and 6 months of age. Heart weight to body weight ratios (HW:BW) were maximally increased in 8-week males (P!0 . 01), whilst HW:BW in females continued to increase progressively up to 6 months (P!0 . 01). This was despite blood pressure being similarly elevated at both the ages in male and female knockout when compared with wild-type (WT) mice (P!0 . 001). Microarray analysis identified altered gene expression at the earliest steps in the hypertrophy-signalling cascade in Npr1K/K mice, particularly calcium-calmodulin signalling and ion channels, with subsequent changes in the expression of intracellular messengers including protein kinases and transcription factors. Real-time PCR analysis confirmed significant differences in gene expression of ANP, BNP, calmodulin 1, histone deacetylase 7a (HDAC7a), protein kinase C (PKC)i, (GATA) 4, collagen 1, phospholamban and transforming growth factor-b1 in Npr1K/K mice when compared with WT (P!0 . 05). The present study implicates the calmodulin-CaMK-Hdac-Mef2 and PKC-MAPK-GATA4 pathways in Npr1 mediation of cardiac hypertrophy.

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Section: Discussionmentioning

confidence: 99%

Npr1-regulated gene pathways contributing to cardiac hypertrophy and fibrosis

Ellmers¹,

Scott

Piuhola

et al. 2007

Journal of Molecular Endocrinology

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“…67,68 Overall, the observational evidence suggests a neutral or beneficial effect of endogenous testosterone on cardiovascular risk factors in middle-aged and older men. 69 The effects of testosterone therapy on markers of cardiovascular risk in ageing men Hypertension. Testosterone therapy does not influence systolic or diastolic blood pressure readings in placebo-controlled trials.…”

Section: Relationship Of Endogenous Testosterone To Markers Of Cardiomentioning

confidence: 99%

Body composition, metabolic syndrome and testosterone in ageing men

Allan¹,

Strauss

McLachlan

2007

Int J Impot Res

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The ageing process in men is marked by changes in body composition (loss of fat-free mass (FFM) and skeletal muscle, and gain in fat mass (FM)) and is associated with a decline in serum testosterone. Correlations between these aspects of ageing and the acknowledged role of exogenous testosterone in reversing the loss of FFM and gain in FM seen in adult men with congenital or acquired hypoandrogenism have led to the hypothesis that testosterone therapy in ageing men will result in favourable changes in body composition and may improve metabolic status and/or cardiovascular risk. Data from randomized controlled trials of testosterone therapy in ageing men addressing the endpoints of body composition and components of the metabolic syndrome and cardiovascular risk factors are reviewed, and the impact of the increasing prevalence of obesity on these relationships is considered.

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“…With respect to behavior, higher historical rates of smoking, obesity (Calle et al, 1999), and unintentional injury (NCHS, 2006) in addition to lower rates of preventive health care (Doyal, 2001) have contributed to greater male mortality rates. Biologically, differences in the level of various sex hormones between men and women may decrease the risk cardiovascular disease of the latter through favorable changes in blood pressure, serum lipids, insulin and glucose levels (Muller et al, 2003).…”

Section: Disparities In Mortality and Total Life Expectancymentioning

confidence: 99%

Disparities in disability life expectancy in us birth cohorts: The influence of sex and race

Soneji

2006

Biodemography and Social Biology

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Racial and sex disparities in chronic diseases and mortality are sources of health inequality and have been observed from infancy to adulthood. Disparities in health and mortality contribute to corresponding disparities in healthy life. I address two previously unanswered questions in the aging literature. First, does the racial and sex gap in healthy life narrow, persist, or expand over age and time, particularly considering severity of ill health, among the oldest old? Second, do some race-sex groups of birth cohorts live not just longer lives, but longer healthier lives, while others spend additional years in illness? To estimate the quantities, I employ a refined definition of physical disability and apply a new extension of Sullivan's method to true birth cohorts. The results suggest among the oldest old, few racial or sex disparities exist over age and time in mild disability. Yet, racial and sex disparities persist over age and time in severe disability.

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Endogenous Sex Hormones and Cardiovascular Disease in Men

Cited by 118 publications

References 143 publications

Npr1-regulated gene pathways contributing to cardiac hypertrophy and fibrosis

Npr1-regulated gene pathways contributing to cardiac hypertrophy and fibrosis

Body composition, metabolic syndrome and testosterone in ageing men

Disparities in disability life expectancy in us birth cohorts: The influence of sex and race

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