MECHANISMS OF ACTION OF TRANSIENT POTENTIAL RECEPTORS (TRP) CHANNELS: RELEVANCE FOR VASCULAR AGING AND MENOPAUSE
FRANCIELY OLIVEIRA DE LIMA e orientado por THAÍS PORTO RIBEIRO e orientado por THAÍS PORTO RIBEIRO
Summary: The vascular effects of estrogen are affected by the stage of reproductive life, the time since menopause, and the extent of cardiovascular diseases (CVD) have been describe. The vascular longevity increase impairing the vascular function as well the hormone loss in menopause process age related, and both are non-modifiable risk factors, which lead to endothelial dysfunction for decrease of protective mechanisms of endothelial cells function. However, the mechanisms of vascular responsiveness to sex steroids during CVD development remain poorly understood in women and men. The aim of this review was to compare a search in the literature about the molecular mechanisms involved in endothelial dysfunction caused by aging-induced menopause and the TRPV4 role. For this, an exploratory and study carried out from searches in the databases: medline and pubmed, where we selected recent studies about this subject matter. Sexual hormones have mechanisms of action described as protectors of resistance mechanisms to stress and their reduction with menopause can aggravate the damages of the aging. Among the adverse mechanisms of endothelial cellular aging are the increase of oxidative stress, inflammation, reduction of NO bioavailability, autophagic flow reduction, mitochondrial dysfunction and alterations of cellular metabolism control pathways. In addition, Transient Potential Receptors (TRP) channels such as TRPV4 channels presents in the endothelial cells membranes may also have protective role during aging-related menopause by interacting with various intracellular proteins. The mechanisms by which the hormonal function and the TRPV4 channels can interfere with the resistance processes to cellular stress or how they may be altered during the process of menopausal aging are not still elucidated by the studies described in the literature. Therefore, the information available up to the present time so that the hypotheses raised on this subject later clarified from preclinical and clinical studies, thus being the basis for improved assistance in the dysfunctions caused by the menopause associated with aging. From this, we can conclude that to understand the mechanisms of this change is important for targeting new preventive and therapeutic strategies such as control endothelial dysfunction and others molecules alterations results of menopause aging process which can lead to more incidence of CVD in women.
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