Francisco Javier Cubero Palero

I graduated in the Universidad Complutense Madrid (UCM) and started my predoctoral stage as a student-collaborator in Dr. Rosa Maria Arahuetes’s lab, granted with a Fellowship from the Regional Government of Madrid. During this period, I began a profitable collaboration with Dr. Paloma Maganto, at the Service of Experimental Surgery in Puerta de Hierro Hospital. I focused his MSc thesis on the expression of bilirubin UDP-glucuronosyl
transferase throughout fetal development. With the financial support of a predoctoral fellowship of the Spanish FISS (ISCIII), I then studied hepatocyte transplantation as an alternative to orthotopic liver transplant in liver-based inborn errors of metabolism, such as the Crigler-Najjar syndrome type I. The doctoral thesis, outstanding cum laude, was titled “Intrasplenic transplantation of hepatocytes in an experimental model of type I Crigler-Najjar syndrome”.

My postdoctoral experience began at Trinity College Dublin in Anatomy and Physiology under the Supervision of Prof. Gabrielle McKee (2004-2006). Later, I joined Dr. Natalia Nieto’s lab, in the Division of Liver Diseases at Mount Sinai School of Medicine as a postdoctoral fellow first and then as a recipient of a postdoctoral fellowship from the Spanish Ministry of Science and Education (Beca MEC/Fulbright), under the auspices of Prof. Scott Friedman. Using his expertise in primary hepatocyte isolation (both fetal and adult), experimentally approached the study of the pathophysiology of alcohol-induced liver fibrosis (2006-2009).

In 2009, I joined the research group headed by Prof. Trautwein (University Hospital RWTH Aachen, Germany) who is an international expert on the functional relevance of cell-type specific signaling pathways in animal models of liver injury and where I became Research Associate (2009-2016).
Since June 2016, I am a Ramon y Cajal Researcher in the Department of Immunology, Ophthalmology and ENT at the Complutense University School of Medicine. My research is focused on endoplasmic reticulum stress as a result of acute (eg: DILI, ALF) and chronic liver disease (MAFLD/AFLD, MASH/MAFLD and end-stage liver carcinogenesis).