PhD (2004) in Pharmacy (Biochemistry), Universidade de Lisboa
Assistant Professor, Biochemistry and Human Biology
Faculdade de Farmácia, Universidade de Lisboa — Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal
Castro research interest’s concerns the homocysteine metabolism, genetic and non-genetic determinants of hyperhomocysteinemia, and the understanding of the molecular mechanisms through which hyperhomocysteinemia causes endothelial dysfunction and vascular disease. Her work in this area have been showing that homocysteine indirectly modulates DNA, RNA and protein methylation patterns, via accumulation of its metabolic precursor, S-adenosylhomocysteine (SAH), a negative regulator of most cell methyltransferases.
Barroso M, Handy DE, Castro R. The link between hyperhomocysteinemia and hypomethylation: implications for cardiovascular disease. J Inborn Errors of Metabolism and Screening (JIEMS) 2017; 5:1-15.
Barroso M, Kao D, Blom HJ, Tavares de Almeida I, Castro R, Loscalzo J, Handy DE. S-adenosylhomocysteine induces inflammation through NFkB: A possible role for EZH2 in endothelial cell activation. Biochim Biophys Acta 2016; 1862:82-92.
Barroso M, Florindo F, Kalwa H, Silva Z, Turanov AA, Carlson BA, Tavares de Almeida I, Blom HJ, Gladyshev VN, Hatfield DL, Michel T, Castro R, Loscalzo J, Handy DE. Inhibition of cellular methyltransferases promotes endothelial cell activation by suppressing glutathione peroxidase-1 expression. J Biol Chem 2014; 289: 15350-62.
Esse R, Imbard A, Florindo C, Gupta S, Quinlivan EP, Davids M, Teerlink T, Tavares de Almeida I, Kruger WD, Blom HJ, Castro R. Protein arginine hypomethylation in a mouse model of cystathionine ß-synthase deficiency. FASEB J 2014; 28:2686-95.
Handy DE, Castro R, Loscalzo J. Epigenetic Modifications: Basic Mechanisms and Role in Cardiovascular Disease. Circulation 2011; 123: 2145-56.