Juan Miguel Redondo

Juan Miguel Redondo Moya
Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid
Project Leader

Nitric Oxide signaling and proteoglycans in Marfan syndrome’s aortopathy: mechanisms and new therapeutic drugs.

• Miguel R. Campanero García
  Consejo Superior de Investigaciones Científicas (CSIC), Madrid

We have defined how NO signaling and proteoglycans accumulation cause Marfan aortopathy and identified new therapeutic targets and biomarkers for disease diagnosis, treatment, and clinical trial monitoring. More specifically we have found that NO overproduction drives aortic disease in Marfan syndrome by overactivating soluble guanylate cyclase (sGC) and cGMP-dependent protein kinase (PKG) , and we show that Versican (VCAN) proteoglycan accumulates in the aorta of MFS patients and mice causing aortopathy via AKT activation. Our results identify not only identify sGC, PKG, AKT and VCAN as mediators and targets for therapeutic intervention in MFS, and also identify a number of potential biomarkers for monitoring MFS aortic disease severity and clinical trials follow-up.

Juan Miguel Redondo is a Full Professor at the Spanish Cardiovascular Research Centre (CNIC). After getting his PhD in Biochemistry and Molecular Biology at the Severo Ochoa Molecular Biology Centre (CBMSO) and obtaining the Extraordinary Prize for Doctoral Thesis, he worked on the generation of diversity and activation of T cell receptors at the Harvard Medical School, Duke Medical Center and the Hospital de la Princesa (Madrid). He then started his own laboratory at the CBMSO in 1995, where he is also a CSIC Full Professor. Juan Miguel joined the CNIC in 2001, he was one of the co-founding members, participating in its development since its inception and serving as Director of the Department of Vascular Biology and Inflammation from 2010 to 2015. He currently leads the laboratory of Gene regulation in Cardiovascular Remodelling and Inflammation Laboratory of the CNIC. (Read full CV).

His work aims to identify new genes that mediate aortic diseases, and new mechanisms and mediators of aortic diseases. The group has pioneered the discovery of novel genes that mediate aortic disease, including Adamts1, Rcan-1, Nos2 C/EBPβ, and Plk1, and of mechanisms showing that syndromic aortic diseases are mediated by overactivation of the NO- sGC-PRKG in mice and patients with Marfan syndrome (MFS). These studies contribute to the understanding of the pathophysiology of thoracic aortic aneurysm and dissection and the identification of biomarkers and therapeutic targets in aortic diseases.

Centro Nacional de Investigaciones Cardiovasculares Carlos III (F.S.P.)
Melchor Fernández Almagro, 3
28029 Madrid
Tel.: (+34) 91 453 12 00 (ext 1150)

Email: [email protected]