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1.
Cells ; 11(2)2022 01 11.
Artículo en Inglés | MEDLINE | ID: mdl-35053356

RESUMEN

The incidence and prevalence of diabetes mellitus (DM) are increasing worldwide, and the resulting cardiac complications are the leading cause of death. Among these complications is diabetes-induced cardiomyopathy (DCM), which is the consequence of a pro-inflammatory condition, oxidative stress and fibrosis caused by hyperglycemia. Cardiac remodeling will lead to an imbalance in cell survival and death, which can promote cardiac dysfunction. Since the conventional treatment of DM generally does not address the prevention of cardiac remodeling, it is important to develop new alternatives for the treatment of cardiovascular complications induced by DM. Thus, therapy with mesenchymal stem cells has been shown to be a promising approach for the prevention of DCM because of their anti-apoptotic, anti-fibrotic and anti-inflammatory effects, which could improve cardiac function in patients with DM.


Asunto(s)
Cardiomiopatías Diabéticas/terapia , Trasplante de Células Madre Mesenquimatosas , Animales , Ensayos Clínicos como Asunto , Cardiomiopatías Diabéticas/genética , Cardiomiopatías Diabéticas/fisiopatología , Epigénesis Genética , Humanos , Modelos Biológicos , Remodelación Vascular
2.
Int J Mol Sci ; 22(2)2021 Jan 07.
Artículo en Inglés | MEDLINE | ID: mdl-33430254

RESUMEN

Estrogen receptors (ER) mediate functions beyond their endocrine roles, as modulation of cardiovascular, renal, and immune systems through anti-inflammatory and anti-apoptotic effects, preventing necrosis of cardiomyocytes and endothelial cells, and attenuating cardiac hypertrophy. Estradiol (E2) prevents cardiac dysfunction, increases nitric oxide synthesis, and reduces the proliferation of vascular cells, yielding protective effects, regardless of gender. Such actions are mediated by ER (ER-alpha (ERα), ER-beta (ERß), or G protein-coupled ER (GPER)) through genomic or non-genomic pathways, which regulate cardiovascular function and prevent tissue remodeling. Despite the extensive knowledge on the cardioprotective effects of estrogen, clinical studies conducted on myocardial infarction (MI) and cardiovascular diseases still include favorable and unfavorable profiles. The purpose of this review is to provide up-to-date information regarding molecular, preclinical, and clinical aspects of cardiovascular E2 effects and ER modulation as a potential therapeutic target for the treatment of MI-induced cardiac dysfunction.


Asunto(s)
Estradiol/uso terapéutico , Receptor alfa de Estrógeno/genética , Receptor beta de Estrógeno/genética , Infarto del Miocardio/tratamiento farmacológico , Animales , Células Endoteliales/metabolismo , Células Endoteliales/patología , Estrógenos/genética , Estrógenos/metabolismo , Femenino , Humanos , Infarto del Miocardio/genética , Infarto del Miocardio/patología , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Receptores de Estrógenos/genética , Receptores Acoplados a Proteínas G/genética
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