F. Xavier Palomer Tarridas
The researcher F. Xavier Palomer Tarridas graduated in Biology in 1995 from the University of Barcelona. In 1998, after receiving a grant from the Ministry of Education and Science, the Researcher began his doctoral studies at the Institute of Molecular Biology in Barcelona (IBMB-CSIC), obtaining his title of Doctor of Biology by the same University of Barcelona in 2002. During that period, he spent a four-month pre-doctoral stay at the Plant Research International technology center in Wageningen (Netherlands), thanks to a BAC grant awarded by UNESCO.
Between 2002 and 2005, the Researcher spent a post-doctoral stay at the current Biomedical Research Institute of the Hospital de la Santa Creu i Sant Pau in Barcelona, where he began the study of metabolic diseases such as type 2 diabetes (DM2) and obesity, but also of autoimmune origin (type 1 diabetes, DM1), both from a clinical and basic perspective.
In 2006, he obtained a post-doctoral contract from the Juan de la Cierva Program (Ministry of Education and Science) to join the research group of Dr. Manuel Vázquez Carrera, of the Department of Pharmacology, Toxicology and Therapeutic Chemistry of the Faculty of Pharmacy and Food Sciences of the University of Barcelona. Between 2008 and 2015 he pursued these post-doctoral studies in the same Department, thanks to the granting of a post-doctoral contract by CIBERDEM (Carlos III Health Institute). In this center, the Researcher continued the study of metabolic diseases with an inflammatory background (obesity and DM2), also initiating research within the line of diabetic cardiomyopathy, which is currently still the subject of his main line of research.
Since 2015 he has been an Associate Professor at the University of Barcelona in the same Department of Pharmacology, Toxicology and Therapeutic Chemistry.
- Barroso E, Rodríguez-Rodríguez R, Zarei M, Pizarro-Degado J, Planavila A, Palomer FX, Villarroya F and Vazquez M SIRT3 deficiency exacerbates fatty liver by attenuating the HIF1a-LIPIN 1 pathway and increasing CD36 through Nrf2. CELL COMMUN SIGNAL . 18(1): 147-147.
- Zarei M, Pizarro J, Barroso E, Palomer FX and Vazquez M Targeting FGF21 for the Treatment of Nonalcoholic Steatohepatitis. TRENDS PHARMACOL SCI . 41(3): 199-208.
- Palomer FX, Román-Azcona MS, Pizarro J, Planavila A, Villarroya F, Valenzuela-Alcaraz BI, Crispi F, Sepúlveda-Martínez Á, Miguel-Escalada I, Ferrer J, Nistal JF, García R, Davidson MM, Barroso E and Vazquez M SIRT3-mediated inhibition of FOS through histone H3 deacetylation prevents cardiac fibrosis and inflammation. signal transduction and targeted therapy . 5(1): 14-14.