Oscar Casis

Background

About Oscar Casis

My research experience started while I was undergraduate student. I worked at the Laboratory of Neurochemistry in Bilbao as an Assistant Student. Just after my graduation, I moved to the Superior Council of Scientific Research (CSIC) in Madrid, where I worked at Dr. J. Tamargo’s lab for 18 months and I learned cardiac cellular electrophysiology and pharmacology. Then, I moved to Dr. J.A. Sánchez-Chapula’s lab at the University of Colima, in México, where I improved my skills in patch-clamp and the physiology and pharmacology of ion channels during 13 months. Came back to Spain I set up the Cellular electrophysiology lab at the Universidad del País Vasco UPV/EHU, where I am the PI until today. During these years, I moved for six months stays to different international laboratories: To the University of Utah, USA, to learn with Dr. Mike Sanguinetti the behavior of hERG channels. To the Federal University of Rio de Janeiro, Brazil, to learn with Dr. Emiliano Medei about cardio-immunology. And, to the Institute du Torax in nantes, France, to learn at Dr. Flavien Charpentier’s lab how to differentiate human induced pluripotent stem cells into cardiac myocytes (hiPS-CMs). In 1994 I started the Electrophysiology Lab at the University of the Basque Country, UPV/EHU. Since then, our focus were: Regulation of cardiac ion channels in both physiological conditions: We demonstrate that there are two Kv4.3 channel populations in cardiac myocytes. One population localized in planar membrane rafts regulated by CaMKII and other population in caveolae regulated by PKA. This line of research yield 11 publications with a cumulative IF > 40 with over 340 citations. Regulation of cardiac ion channels in endocrine diseases: Diabetic cardiomyopathy induced a proarrhythmic electrical remodeling, caused mainly by the elevated circulating cytokines that can be prevented by blocking the Kv1.3 channel. Besides, the proarrhythmic electrical remodeling induced by hypothyrioidism is partially due to a direct effect of TSH on the heart. In this line, we published 19 papers with a cumulative IF > 80, that have been cited near 600 times. Molecular mechanisms of cardiac arrhythmias: we demonstrated for the very first time that mutations in accessory beta subunits of the Ca+2 and Na+ channels can cause short QT or Brugada syndromes. This line of research yield 9 publications with cumulative IF > 50 cited more than 1400 times. Other lines: we participated in collaborations and other lines of research that yield more than 60 publications, with an h index of 24, cited near times.