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Renal health
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CKD exhibits a higher prevalence in women compared to males, despite a larger proportion of males receiving nephrological care. Female CKD patients have less likelihood of progressing to ESRD and lower risks of CV events and mortality. Gender differences in CKD are influenced by oxidative stress, inflammation, apoptosis, and renal hemodynamics, with estrogen providing protective effects and testosterone exacerbating renal injury. Transgender hormone therapies impact kidney health, with significant changes observed in serum creatinine levels, particularly in transgender women.
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The specific mechanisms underlying the gender disparities observed in CKD prevalence, progression to ESRD, and treatment outcomes. The comprehensive effects of gender-affirming hormone therapy on kidney function. The long-term effects of testosterone therapy on renal function in transgender men. The detailed molecular pathways through which estrogen and testosterone modulate oxidative stress, inflammation, apoptosis, and renal hemodynamics in CKD.
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Conduct longitudinal studies to evaluate the long-term effects of GAHTs on renal function in transgender individuals. Explore the potential mechanisms provoking changes in renal function during testosterone therapy of transgender men, develop strategies for mitigating risks. Investigate the underlying molecular mechanisms driving gender disparities in CKD prevalence, progression, and treatment outcomes to develop personalized treatments. Elucidate the molecular pathways through which estrogen and testosterone influence oxidative stress, inflammation, apoptosis, and renal hemodynamics in CKD.
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Cardiac health
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Estrogen inhibits cardiomyocyte hypertrophy, enhances mitochondrial activity, prevents apoptosis, promotes cardiac regeneration, and modulates cardiac electrical conductance, potentially contributing to a lower incidence of HF and delayed onset of IHD in women. Androgens have pro-hypertrophic effects, induce cardiomyocyte apoptosis, and increase oxidative stress, possibly contributing to a higher likelihood of HF in males and earlier onset of IHD.
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AR subtypes on the surface of and inside cardiomyocytes. The relationship between hormonal imbalances and the development and progression of HF, as well as the impact of HF on hormonal imbalances. The reasons behind the delayed onset of IHD in women compared to males and the potential molecular mechanisms underlying estrogen’s cardioprotective effects.
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Clinical trials to assess the CV effects of HRT in postmenopausal women, considering different hormone formulations, dosages, and patient characteristics. Advanced preclinical models to study sex-specific cardiac responses and test potential therapeutic interventions. Elucidate the molecular mechanisms underlying estrogen’s cardioprotective effects against IHD and investigate potential therapeutic interventions.
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Vascular health
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Premenopausal women have lower blood pressure and lower incidence of ASCVD compared to age-matched men, but the prevalence increases in postmenopausal women. Estrogen promotes vasodilation and vascular remodeling, decreases migration and proliferation of VSMC. It increases the RAS components that oppose increased blood pressure and enhances βAR-induced vasorelaxation in SNS. It also controls lipid metabolism, inflammation, and plaque stability to mitigate ASCVD progression. Androgens may provoke both vasodilation and vasoconstriction. They increase the vasoconstrictor components of RAS and promote αAR-induced vasoconstriction.
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AR subtypes on the surface of and inside vascular cells. Detailed molecular pathways through which estrogen and androgens modulate vascular cell function, macrophage polarization, endothelial function, and plaque stability. The role of progesterone in CV health and its potential to counteract estrogen’s cardioprotective effects. Research on other sex hormones, such as DHEA-S, and their influence on atherosclerosis pathophysiology and clinical outcomes.
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Include diverse populations in future clinical trials of ASCVD and HTN and consider stratification by sex, age, menopausal status, and CV risk factors. Studies on the long-term atherosclerotic and hypertensive effects of GAHTs in transgender individuals, stratifying by hormone regimen, duration of treatment, and other health factors. Advanced preclinical models to investigate sex-specific vascular respons es in HTN and ASCVD. Elucidate molecular mechanisms underlying the effects of estrogen and androgen on vascular cells in HTN and ASCVD.
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Obesity
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Testosterone is associated with lower triglyceride levels and estrogen potentially lowers total cholesterol levels. Sex hormones influence adipose tissue distribution as men tend to accumulate visceral fat and women subcutaneous fat. Testosterone and estrogen treatments influence insulin sensitivity in animal models.
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Exact molecular mechanisms underlying sex hormones’ effects in obesity-related conditions. The long-term effects of sex hormone therapies on metabolic health and CV outcomes. Variability in response to sex hormone therapies among individuals. Potential role of gut microbiota in mediating the effects of sex hormones on obesity and metabolic health.
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Investigate the mechanisms underlying the sex-specific differences in fat distribution and its implications for metabolic health. Investigate the interaction between sex hormones and genetics, environmental factors in obesity and metabolic syndrome. Evaluate the efficacy and safety of gender-tailored interventions for obesity prevention and management.
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