Enrique Lara-Pezzi graduated in Chemistry from the Universidad Autónoma de Madrid (1995) and obtained his PhD in Biochemistry and Molecular Biology from the same University in 2000.
During his PhD, carried out in Dr. López-Cabrera's laboratory at the Hospital Universitario de la Princesa in Madrid, Spain (1995-2000), he focused on the study of the HBx protein of the hepatitis B virus and its contribution to the immune response and the development of hepatocellular carcinoma.
After a first postdoctoral stay at Dr. López-Cabrera's laboratory, during which he continued the study of the HBx protein, he joined the laboratory of Prof. Nadia Rosenthal (European Molecular Biology Laboratory, Monterotondo, Italy) to study the contribution of the calcineurin isoform CnAβ1 to skeletal muscle regeneration (2003-2006). Sponsored by the Marie Curie Programme, he moved to Prof. Rosenthal's laboratory at the Heart Science Centre (Imperial College London) to investigate the molecular mechanisms that mediate heart failure and cardiac regeneration (2006-2009).
In 2009 he joined the Spanish National Centre for Cardiovascular Research (CNIC) as a group leader. He is also an honorary fellow of the Faculty of Medicine at Imperial College London, where he studies the molecular mechanisms of heart failure, recovery and regeneration.
Our lab studies the molecular mechanisms that regulate heart disease. One of the main interests in our lab is the calcineurin variant CnAβ1. Calcineurin regulates a wide variety of physiological and pathological processes, including cardiac development and hypertrophy. CnAβ1 is a naturally occurring splicing variant of the calcineurin A gene with a unique C-terminal region, different from the autoinhibitory domain present in all CnA isoforms. We have recently shown that CnAβ1 regulates cell proliferation and enhances skeletal muscle regeneration. In the heart, our results suggest that CnAβ1 compensates cardiac atrophy and, more importantly, protects from the deleterious effects of myocardial infarction, reducing inflammation and scar formation.
Our lab also studies the role of follistatin-like molecules Fstl1 and Fstl3 during heart remodelling and failure following cardiac hypertrophy or myocardial infarction. We have recently described that both Fstl1 and Fstl3 are induced in the failing myocardium. We are currently investigating the role of these molecules by using knock-out and transgenic mice together with cell cultures and different molecular biology approaches.