Graduated with honors in Biology, Health and Biotechnology, with specialization in pathophysiology at the Institute of Cardiovascular and Metabolic Diseases (Toulouse, France). His PhD projects dealt with different aspects of heart failure and lung diseases to identify new therapeutic targets and strategies. During his early research career, Dr. Bisserier has identified new Epac inhibitors and provided new alternatives for treating patients with heart failure or cancer. He also investigated for the first time the role of Carabin in cardiac hypertrophy and heart failure and identified a new therapeutic target. At the Institute of Cardiology and Pneumology of Quebec (Canada), he investigated the molecular and cellular mechanisms involved in vascular and bronchial remodeling using a translational approach (from genetics to the animal experiments). At the Department of Pathology at Yale University (Connecticut, United States), he investigated the role of pro-survival pathways and acquired-mutations of the EZH2 gene in conferring resistance to the EZH2 inhibitors-targeted therapies in Lymphoma. In 2017, Dr. Bisserier accepted a new position in the Department of Cardiology at the Cardiovascular Research Center, at Mount Sinai (New York, United States) and initiated new studies on the identification and characterization of innovative therapeutic targets in lung diseases.
Now, his specific research areas focuses on vascular physiopathology and gene transfer for treating pulmonary arterial hypertension (PAH), lung fibrosis and heart failure at the Cardiovascular Research Center, Mount Sinai, New York. Despite extensive research efforts in experimental and clinical studies, PAH and lung fibrosis remain an increasing cause of morbidity and mortality. There is a compelling need to develop more effective and reliable therapeutic. Therefore, his current research interest includes: 1. Regulation of gene-expression in PAH. 2. Identification of novel therapeutic strategies in pulmonary diseases, vascular remodeling diseases and heart failure by using targeted-gene therapy