Abstract
Metabolic syndrome (MS) is characterized by the convergence of several risk factors at the same time in which each individual contributes to cardiovascular risk. Although the factors that establish the relationship between metabolic alterations and vascular changes that predispose to cardiovascular events are not fully understood, it is likely that endothelial dysfunction has decisive importance in this regard. We implemented the use of fibrinogen, nitric oxide, adiponectin, and superoxide dismutase, to evaluate the implication of these phenomena in mitochondrial function and morphology in a MS model. It was demonstrated that the sustained oxidative stress situation induces histological alterations at the aortic level. This pathological and oxidative state leads to a mitochondrial dysfunction with repercussion in the morphology of this organelle.
Due to the intimate link to insulin resistance (IR), obesity, and MS, the importance of studying the implication of the inflammatory phenomenon and associated oxidative stress is understood, in order to establish the probable physiopathogenic mechanisms with the aim of generating strategies that prevent the incidence and prevalence of this pathology, given that it has huge consequences in health system. For this it is necessary to identify the determinants of the disease in order to implement preventive measures for control and monitoring as well as to study therapeutic strategies that can be implemented to reduce the incidence of this multisyndromic pathology.
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del Carmen Baez, M., Tarán, M., Moya, M., de la Paz Scribano Parada, M. (2019). Oxidative Stress in Metabolic Syndrome: Experimental Model of Biomarkers. In: Chakraborti, S., Dhalla, N., Dikshit, M., Ganguly, N. (eds) Modulation of Oxidative Stress in Heart Disease. Springer, Singapore. https://doi.org/10.1007/978-981-13-8946-7_12
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