RESUMEN
Aging is an important risk factor for the development of heart failure (HF) and half of patients with HF have preserved ejection fraction (HFpEF) which is more common in elderly women. In general, sex differences that lead to discrepancies in risk factors and to the development of cardiovascular disease (CVD) have been attributed to the reduced level of circulating estrogen during menopause. Estrogen receptors adaptively modulate fibrotic, apoptotic, inflammatory processes and calcium homeostasis, factors that are directly involved in the HFpEF. Therefore, during menopause, estrogen depletion reduces the cardioprotection. Preclinical menopause models demonstrated that several signaling pathways and organ systems are closely involved in the development of HFpEF, including dysregulation of the renin-angiotensin system (RAS), chronic inflammatory process and alteration in the sympathetic nervous system. Thus, this review explores thealterations observed in the condition of HFpEF induced by menopause and the therapeutic targets with potential to interfere with the disease progress.
Asunto(s)
Insuficiencia Cardíaca , Femenino , Humanos , Masculino , Anciano , Insuficiencia Cardíaca/metabolismo , Volumen Sistólico/fisiología , Menopausia , Sistema Renina-Angiotensina , Estrógenos/uso terapéuticoRESUMEN
Stem cell therapy is a promising alternative approach to heart diseases. The most prevalent source of multipotent stem cells, usually called somatic or adult stem cells (mesenchymal stromal/stem cells, MSCs) used in clinical trials is bone marrow (BM-MSCs), adipose tissue (AT-MSCs), umbilical cord (UC-MSCs) and placenta. Therapeutic use of MSCs in cardiovascular diseases is based on the benefits in reducing cardiac fibrosis and inflammation that compose the cardiac remodeling responsible for the maintenance of normal function, something which may end up causing progressive and irreversible dysfunction. Many factors lead to cardiac fibrosis and failure, and an effective therapy is lacking to reverse or attenuate this condition. Different approaches have been shown to be promising in surpassing the poor survival of transplanted cells in cardiac tissue to provide cardioprotection and prevent cardiac remodeling. This review includes the description of pre-clinical and clinical investigation of the therapeutic potential of MSCs in improving ventricular dysfunction consequent to diverse cardiac diseases.
Asunto(s)
Fibrosis/terapia , Cardiopatías/terapia , Trasplante de Células Madre Mesenquimatosas/métodos , Células Madre Mesenquimatosas/citología , Animales , HumanosRESUMEN
Bicuspid aortic valve (BAV) is associated with annuloaortic ectasia, dissection and ascending aortic aneurysm. The high incidence of this congenital malformation and aortic disease suggests a close correlation between the two phenomena. Abnormalities in different phases of cell migration of the neural crest might be responsible for the occurrence of abnormalities in the aortic valve, media layer of the ascending aorta and vessels of the aortic arch. Previous studies have shown that patients with normal BAV or slight dysfunction may present with dilation of the aortic root. The hemodynamic changes caused by BAV without stenosis or insufficiency seem to be an insufficient explanation for these findings. Several mechanisms have been proposed to explain the molecular and hystological aspects of this disease. We found a reduced fibrillin-1 content in both ascending aorta and pulmonary trunk as a possible cause. Histologically, the ascending aorta can present cystic medial necrosis and elastic fragmentation, similar to Marfan's disease. Some authors concluded that many patients, mainly those with aortic regurgitation, should have the aortic valve and the ascending aorta replaced at the same procedure, even if a mild dilatation (45 mm) is present in patients with BAV if life expectancy is anticipated to be greater than 10 years to prevent further aneurysms or ruptures.