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9 results on '"Blanco, Eva M."'

1. Tromboendarterectomía pulmonar en pacientes con hipertensión pulmonar tromboembólica crónica y afectación distal

Author

Gotor-Pérez, Consuelo A., López-Gude, María J., Benito-Arnaiz, Victoria, Pérez de la Sota, Enrique, Centeno-Rodríguez, Jorge E., Eixerés-Esteve, Andrea, Aguilar-Blanco, Eva M., Barajas-Díaz, Carolina, Velázquez-Martín, María T., Pérez-Núñez, Marta, Pérez-Vela, José L., Escribano-Subías, Pilar, and Cortina-Romero, José M.

Published
2020
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2. Extracellular Tuning of Mitochondrial Respiration Leads to Aortic Aneurysm

Author

Instituto de Salud Carlos III, European Commission, Comunidad de Madrid, Instituto de Investigación Hospital 12 de Octubre, Oller, Jorge, Gabandé-Roldríguez, Enrique, Ruíz-Rodríguez, María J., Desdín-Mico, Gabriela, Aranda, Juan Francisco, Rodriguez-Díez, Raquel, Ballesteros-Martínez, Constanza, Blanco, Eva M., Roldan-Montero, Raquel, Acuña, Pedro, Forteza Gil, Alberto, Martín-López, Carlos E., Nistal, J. Francisco, Lino Cardenas, Christian L, Lindsay, Mark Evan, Martín-Ventura, Jose Luis, Briones, Ana M., Miguel Redondo, Juan, Mittelbrunn, María, Instituto de Salud Carlos III, European Commission, Comunidad de Madrid, Instituto de Investigación Hospital 12 de Octubre, Oller, Jorge, Gabandé-Roldríguez, Enrique, Ruíz-Rodríguez, María J., Desdín-Mico, Gabriela, Aranda, Juan Francisco, Rodriguez-Díez, Raquel, Ballesteros-Martínez, Constanza, Blanco, Eva M., Roldan-Montero, Raquel, Acuña, Pedro, Forteza Gil, Alberto, Martín-López, Carlos E., Nistal, J. Francisco, Lino Cardenas, Christian L, Lindsay, Mark Evan, Martín-Ventura, Jose Luis, Briones, Ana M., Miguel Redondo, Juan, and Mittelbrunn, María

Abstract

Marfan syndrome (MFS) is an autosomal dominant disorder of the connective tissue caused by mutations in the FBN1 (fibrillin-1) gene encoding a large glycoprotein in the extracellular matrix called fibrillin-1. The major complication of this connective disorder is the risk to develop thoracic aortic aneurysm. To date, no effective pharmacologic therapies have been identified for the management of thoracic aortic disease and the only options capable of preventing aneurysm rupture are endovascular repair or open surgery. Here, we have studied the role of mitochondrial dysfunction in the progression of thoracic aortic aneurysm and mitochondrial boosting strategies as a potential treatment to managing aortic aneurysms.

Published
2021

3. Deletion of delta-like 1 homologue accelerates renal inflammation by modulating the Th17 immune response

Author

Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Comunidad de Madrid, Fondo Nacional de Desarrollo Científico y Tecnológico (Chile), Márquez-Expósito, Laura, Rodrigues-Diez, Raul R., Rayego-Mateos, Sandra, Fierro-Fernández, Marta, Rodrigues-Díez, Raquel, Orejudo, Macarena, Santos-Sánchez, Laura, Blanco, Eva M., Laborda, Jorge, Mezzano, Sergio, Lamas, Santiago, Lavoz, Carolina, Ruíz-Ortega, Marta, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Comunidad de Madrid, Fondo Nacional de Desarrollo Científico y Tecnológico (Chile), Márquez-Expósito, Laura, Rodrigues-Diez, Raul R., Rayego-Mateos, Sandra, Fierro-Fernández, Marta, Rodrigues-Díez, Raquel, Orejudo, Macarena, Santos-Sánchez, Laura, Blanco, Eva M., Laborda, Jorge, Mezzano, Sergio, Lamas, Santiago, Lavoz, Carolina, and Ruíz-Ortega, Marta

Abstract

Preclinical studies have demonstrated that activation of the NOTCH pathway plays a key role in the pathogenesis of kidney damage. There is currently no information on the role of the Delta-like homologue 1 (DLK1), a NOTCH inhibitor, in the regulation of renal damage. Here, we investigated the contribution of DLK1 to experimental renal damage and the underlying molecular mechanisms. Using a Dlk1-null mouse model in the experimental renal damage of unilateral ureteral obstruction, we found activation of NOTCH, as shown by increased nuclear translocation of the NOTCH1 intracellular domain, and upregulation of Dlk2/hey-1 expression compared to wild-type (WT) littermates. NOTCH1 over-activation in Dlk1-null injured kidneys was associated with a higher inflammatory response, characterized by infiltration of inflammatory cells, mainly CD4/IL17A + lymphocytes, and activation of the Th17 immune response. Furthermore, pharmacological NOTCH blockade inhibited the transcription factors controlling Th17 differentiation and gene expression of the Th17 effector cytokine IL-17A and other related-inflammatory factors, linked to a diminution of inflammation in the injured kidneys. We propose that the non-canonical NOTCH ligand DLK1 acts as a NOTCH antagonist in renal injury regulating the Th17-mediated inflammatory response.

Published
2021

5. T cells with dysfunctional mitochondria induce multimorbidity and premature senescence

Author

Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Desdín-Mico, Gabriela, Soto-Heredero, Gonzalo, Aranda, Juan Francisco, Oller, Jorge, Carrasco, Elisa, Gabandé-Rodríguez, Enrique, Blanco, Eva M., Alfranca, Arantzazu, Cussó, Lorena, Desco, Manuel, Ibañez, Borja, Gortazar, Arancha R., Fernández-Marcos, Pablo, Navarro, María N., Hernaez, Bruno, Alcamí, Antonio, Baixauli, Francesc, Mittelbrunn, María, Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Desdín-Mico, Gabriela, Soto-Heredero, Gonzalo, Aranda, Juan Francisco, Oller, Jorge, Carrasco, Elisa, Gabandé-Rodríguez, Enrique, Blanco, Eva M., Alfranca, Arantzazu, Cussó, Lorena, Desco, Manuel, Ibañez, Borja, Gortazar, Arancha R., Fernández-Marcos, Pablo, Navarro, María N., Hernaez, Bruno, Alcamí, Antonio, Baixauli, Francesc, and Mittelbrunn, María

Abstract

The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (“inflammaging”). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-a signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases.

Published
2020

9. Is CorMatrix really a recellularization scaffold as a pericardial substitute in cardiac surgery?

Author

Bustamante-Munguira J, Serrano R, Figuerola-Tejerina A, Aguilar-Blanco EM, and Calzada M

Subjects
Aged, Aortic Valve diagnostic imaging, Aortic Valve physiopathology, Aortic Valve Stenosis diagnostic imaging, Aortic Valve Stenosis physiopathology, Blood Vessel Prosthesis Implantation instrumentation, Device Removal, Endocarditis diagnosis, Endocarditis microbiology, Foreign-Body Reaction etiology, Foreign-Body Reaction pathology, Humans, Male, Prosthesis-Related Infections diagnosis, Prosthesis-Related Infections microbiology, Reoperation, Risk Assessment, Severity of Illness Index, Treatment Outcome, Aortic Valve surgery, Aortic Valve Stenosis surgery, Biocompatible Materials adverse effects, Blood Vessel Prosthesis adverse effects, Blood Vessel Prosthesis Implantation adverse effects, Endocarditis surgery, Extracellular Matrix transplantation, Prosthesis-Related Infections surgery
Published
2018
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