Mercedes Liliana Castro Pinto

Mrs. Mercedes Liliana Castro Pinto

Ramon y Cajal University Hospital, Madrid, Spain
orcid

Research Focus & Metrics

Academic Career Length

6Years (2021-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
31 August 2022 in Antioxidants
Verified
Journal Article
Open access
PDF file
SSsandra Sanchez-esteban
sandra Sanchez-esteban
MPMercedes Liliana Castro Pinto
Mercedes Liliana Castro Pinto
ACAlberto Cook-Calvete
Alberto Cook-Calvete
PRPaula Reventún
Paula Reventún
MDMaría Delgado-Marin
María Delgado-Marin
Marta SauraMarta Saura
Marta Saura
Calcific aortic valve disease (CAVD) is highly prevalent during aging. CAVD initiates with endothelial dysfunction, leading to lipid accumulation, inflammation, and osteogenic transformation. Integrin-linked kinase (ILK) participates in the progression of cardiovascular diseases, such as endothelial dysfunction and atherosclerosis. However, ILK role in CAVD is unknown. First, we determined that ILK expression is downregulated in aortic valves from patients with CAVD compared to non-CAVD, especially at the valve endothelium, and negatively correlated with calcification markers. Silencing ILK expression in human valve endothelial cells (siILK-hVECs) induced endothelial-to-mesenchymal transition (EndMT) and promoted a switch to an osteoblastic phenotype; SiILK-hVECs expressed increased RUNX2 and developed calcified nodules. siILK-hVECs exhibited decreased NO production and increased nitrosative stress, suggesting valvular endothelial dysfunction. NO treatment of siILK-hVECs prevented VEC transdifferentiation, while treatment with an eNOS inhibitor mimicked ILK-silencing induction of EndMT. Accordingly, NO treatment inhibited VEC calcification. Mechanistically, siILK-hVECs showed increased Smad2 phosphorylation, suggesting a TGF-β-dependent mechanism, and NO treatment decreased Smad2 activation and RUNX2. Experiments performed in eNOS KO mice confirmed the involvement of the ILK-eNOS signaling pathway in valve calcification, since aortic valves from these animals showed decreased ILK expression, increased RUNX2, and calcification. Our study demonstrated that ILK endothelial expression participates in human CAVD development by preventing endothelial osteogenic transformation.

30 November 2021 in Metro Ciencia
Verified
Journal Article
Open access
EFEdmundo Fajardo-Rodriguez
Edmundo Fajardo-Rodriguez
JMJavier Miguelena-Hycka
Javier Miguelena-Hycka
JLJose Lopez-Menendez
Jose Lopez-Menendez
MPMercedes Liliana Castro Pinto
Mercedes Liliana Castro Pinto
RPRafael Muñoz Pérez
Rafael Muñoz Pérez
JRJorge Rodriguez-Roda
Jorge Rodriguez-Roda
La perforación tardía de miocardio (PTMI) secundaria a un dispositivo electrónico intracardiaco (DEI), es una complicación poco frecuente pero que puede ser mortal.

30 November 2021 in Metro Ciencia
Verified
Journal Article
Open access
PDF file
EFEdmundo Fajardo-Rodriguez
Edmundo Fajardo-Rodriguez
JLJose Lopez-Menendez
Jose Lopez-Menendez
MPMercedes Liliana Castro Pinto
Mercedes Liliana Castro Pinto
MGMiren Martín García
Miren Martín García
RPRafael Muñoz Pérez
Rafael Muñoz Pérez
JRJorge Rodriguez-Roda
Jorge Rodriguez-Roda
La cirugía de revascularización coronaria (CABG) es el tratamiento más efectivo en la cardiopatía isquémica, siendo la vena safena mayor el injerto más utilizado a nivel mundial. Objetivo. El objetivo principal de este trabajo fue evaluar en los grupos de Duragraft y solución salina heparinizada las incidencias de eventos cardiovasculares mayores (MACES) en una variable compuesta por (Muerte, infarto de miocardio (IM) y nueva revascularización) en un periodo de 12 meses posterior a la cirugía.