Person: Jiménez González, Sara
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First Name
Sara
Last Name
Jiménez González
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Fisiología
Area
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Publication Oxidative Stress and Vascular Damage in the Context of Obesity: The Hidden Guest(MPDI, 2021-03-08) Martínez Martínez, Ernesto; Souza Neto, Francisco; Jiménez González, Sara; Cachofeiro, VictoriaThe vascular system plays a central role in the transport of cells, oxygen and nutrients between different regions of the body, depending on the needs, as well as of metabolic waste products for their elimination. While the structure of different components of the vascular system varies, these structures, especially those of main arteries and arterioles, can be affected by the presence of different cardiovascular risk factors, including obesity. This vascular remodeling is mainly characterized by a thickening of the media layer as a consequence of changes in smooth muscle cells or excessive fibrosis accumulation. These vascular changes associated with obesity can trigger functional alterations, with endothelial dysfunction and vascular stiffness being especially common features of obese vessels. These changes can also lead to impaired tissue perfusion that may affect multiple tissues and organs. In this review, we focus on the role played by perivascular adipose tissue, the activation of the renin-angiotensin-aldosterone system and endoplasmic reticulum stress in the vascular dysfunction associated with obesity. In addition, the participation of oxidative stress in this vascular damage, which can be produced in the perivascular adipose tissue as well as in other components of the vascular wall, is updated.Publication Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress(MDPI, 2022-06-22) Souza Neto, Francisco V.; Islas, Fabián; Jiménez González, Sara; Luaces Méndez, María; Ramchandani, Bunty; Romero Miranda, Ana; Delgado Valero, Beatriz; Roldan Molina, Elena; Saiz Pardo, Melchor; Cerón Nieto, María Ángeles; Ortega Medina, Luis; Martínez Martínez, Ernesto; Cachofeiro Ramos, VictoriaWe have evaluated cardiac function and fibrosis in infarcted male Wistar rats treated with MitoQ (50 mg/kg/day) or vehicle for 4 weeks. A cohort of patients admitted with a first episode of acute MI were also analyzed with cardiac magnetic resonance and T1 mapping during admission and at a 12-month follow-up. Infarcted animals presented cardiac hypertrophy and a reduction in the left ventricular ejection fraction (LVEF) and E- and A-waves (E/A) ratio when compared to controls. Myocardial infarction (MI) rats also showed cardiac fibrosis and endoplasmic reticulum (ER) stress activation. Binding immunoglobulin protein (BiP) levels, a marker of ER stress, were correlated with collagen I levels. MitoQ reduced oxidative stress and prevented all these changes without affecting the infarct size. The LVEF and E/A ratio in patients with MI were 57.6 ± 7.9% and 0.96 ± 0.34, respectively. No major changes in cardiac function, extracellular volume fraction (ECV), or LV mass were observed at follow-up. Interestingly, the myeloperoxidase (MPO) levels were associated with the ECV in basal conditions. BiP staining and collagen content were also higher in cardiac samples from autopsies of patients who had suffered an MI than in those who had died from other causes. These results show the interactions between mitochondrial oxidative stress and ER stress, which can result in the development of diffuse fibrosis in the context of MI.Publication Resultados de una unidad funcional de pie diabético integrada por un podólogo y un endocrinólogo dentro del sistema nacional de salud(Universidad Complutense de Madrid, 2018-10-24) Jiménez González, Sara; Lázaro Martínez, José Luis; Rubio García, José AntonioEl Síndrome de Pie Diabético (PD) es una de las complicaciones más tardía e incapacitante de la Diabetes Mellitus (DM). Diversos posicionamientos científicos, ADA, NICE e IDF, dejan bien establecido que los pacientes con lesiones por PD y los que tienen alto riesgo para ulcerarse, deben ser atendidos por equipos multidisciplinarios. En el año 2008 en el Hospital Universitario Príncipe de Asturias de Alcalá de Henares (Madrid), se puso en funcionamiento una Consulta de Pie Diabético (CPD), atendida por un podólogo y un endocrinólogo para dar cobertura a pacientes con pie diabético. De manera progresiva se ha coordinado con distintas disciplinas implicadas formándose así, una Unidad Funcional de Pie Diabético (UFPD). En este estudio se planteo como hipótesis si la implementación de una UFPD dentro del Sistema Nacional de Salud (SNS), cuyo eje central de funcionamiento se realice por el trabajo coordinado de un podólogo y un endocrinólogo, se asocia con unos resultados favorables en la atención del paciente con PD, como son: (i) tasas de cicatrización similares a unidades de referencia en PD en Europa, (ii) reducción de la tasa de reulceración en la población atendida en la UFPD, (iii) reducción de tasas de amputación mayor en población con DM del área de salud. Para abordar los objetivos se desarrollaron dos estudios independientes pero complementarios. 1) Análisis de los pacientes atendidos en la CPD de la UFPD: se analizaron las características clínicas de la muestra de sujetos, los episodios registrados como úlceras en los pies, la reulceración de los pacientes durante el seguimiento y la mortalidad de los mismos, mediante un estudio retrospectivo de cohortes desde Marzo del 2008 a diciembre del 2014. Se incluyó una muestra final de 345 sujetos que generaron 590 episodios de ulceración. 2) Análisis de incidencia de amputaciones del miembro inferior (AMI) en población con diabetes y sin diabetes mediante un estudio retrospectivo de cohortes de las AMI de causa no traumática que ha tenido lugar en la población censada en nuestra área de salud, desde 1-1-2001 al 31-12-2014...Publication The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats(MPDI, 2021-08-11) Souza Neto, Francisco V.; Jiménez González, Sara; Delgado Valero, Beatriz; Jurado López, Raquel; Genty, Marie; Romero Miranda, Ana; Rodríguez, Cristina; Nieto, María Luisa; Martínez Martínez, Ernesto; Cachofeiro, VictoriaWe have evaluated the role of mitochondrial oxidative stress and its association with endoplasmic reticulum (ER) stress activation in the progression of obesity-related cardiovascular fibrosis. MitoQ (200 µM) was orally administered for 7 weeks to male Wistar rats that were fed a high-fat diet (HFD, 35% fat) or a control diet (CT, 3.5% fat). Obese animals presented cardiovascular fibrosis accompanied by increased levels of extracellular matrix proteins and profibrotic mediators. These alterations were associated with ER stress activation characterized by enhanced levels (in heart and aorta vs. CT group, respectively) of immunoglobulin binding protein (BiP; 2.1-and 2.6-fold, respectively), protein disulfide-isomerase A6 (PDIA6; 1.9-fold) and CCAAT-enhancer-binding homologous protein (CHOP; 1.5- and 1.8-fold, respectively). MitoQ treatment was able to prevent (p < 0.05) these modifications at cardiac and aortic levels. MitoQ (5 nM) and the ER stress inhibitor, 4-phenyl butyric acid (4 µM), were able to block the prooxidant and profibrotic effects of angiotensin II (Ang II, 10−6 M) in cardiac and vascular cells. Therefore, the data show a crosstalk between mitochondrial oxidative stress and ER stress activation, which mediates the development of cardiovascular fibrosis in the context of obesity and in which Ang II can play a relevant role.