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1.
Curr Heart Fail Rep ; 19(4): 200-212, 2022 08.
Artigo em Inglês | MEDLINE | ID: mdl-35624387

RESUMO

PURPOSE OF REVIEW: Sex hormones drive development and function of reproductive organs or the development of secondary sex characteristics but their effects on the cardiovascular system are poorly understood. In this review, we identify the gaps in our understanding of the interaction between sex hormones and the cardiovascular system. RECENT FINDINGS: Studies are progressively elucidating molecular functions of sex hormones in specific cell types in parallel with the initiation of crucial large randomized controlled trials aimed at improving therapies for cardiovascular diseases (CVDs) associated with aberrant levels of sex hormones. In contrast with historical assumptions, we now understand that men and women show different symptoms and progression of CVDs. Abnormal levels of sex hormones pose an independent risk for CVD, which is apparent in conditions like Klinefelter syndrome, androgen insensitivity syndrome, and menopause. Moreover, sex hormone-based therapies remain understudied and may not be beneficial for cardiovascular health.


Assuntos
Doenças Cardiovasculares , Insuficiência Cardíaca , Doenças Cardiovasculares/etiologia , Feminino , Hormônios Esteroides Gonadais/metabolismo , Humanos , Masculino , Menopausa
2.
Int J Mol Sci ; 22(7)2021 Mar 31.
Artigo em Inglês | MEDLINE | ID: mdl-33807195

RESUMO

(1) Background: The exact mechanism(s) underlying pathological changes in a heart in transition to hypertrophy and failure are not yet fully understood. However, alterations in cardiac energy metabolism seem to be an important contributor. We characterized an in vitro model of adrenergic stimulation-induced cardiac hypertrophy for studying metabolic, structural, and functional changes over time. Accordingly, we investigated whether metabolic interventions prevent cardiac structural and functional changes; (2) Methods: Primary rat cardiomyocytes were treated with phenylephrine (PE) for 16 h, 24 h, or 48 h, whereafter hypertrophic marker expression, protein synthesis rate, glucose uptake, and contractile function were assessed; (3) Results: 24 h PE treatment increased expression of hypertrophic markers, phosphorylation of hypertrophy-related signaling kinases, protein synthesis, and glucose uptake. Importantly, the increased glucose uptake preceded structural and functional changes, suggesting a causal role for metabolism in the onset of PE-induced hypertrophy. Indeed, PE treatment in the presence of a PAN-Akt inhibitor or of a GLUT4 inhibitor dipyridamole prevented PE-induced increases in cellular glucose uptake and ameliorated PE-induced contractile alterations; (4) Conclusions: Pharmacological interventions, forcing substrate metabolism away from glucose utilization, improved contractile properties in PE-treated cardiomyocytes, suggesting that targeting glucose uptake, independent from protein synthesis, forms a promising strategy to prevent hypertrophy and hypertrophy-induced cardiac dysfunction.


Assuntos
Cardiomegalia/metabolismo , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/fisiologia , Animais , Animais Recém-Nascidos , Células Cultivadas , Metabolismo Energético , Glucose/metabolismo , Contração Muscular/efeitos dos fármacos , Contração Muscular/fisiologia , Miócitos Cardíacos/efeitos dos fármacos , Fenilefrina/farmacologia , Fosforilação , Ratos , Transdução de Sinais/efeitos dos fármacos
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