Jin O-Uchi

Jin O-Uchi, MD, PhD

Contact Dr. O-Uchi

1020 Locust Street
Room 543G
Philadelphia, PA 19107

(215) 503-5616
(215) 503-5731 fax

Medical School

The Jikei University School of Medicine, Tokyo Japan - 2001

Residency

Jikei University Hospital, Tokyo, Japan, 2001-2003

Fellowship

Postdoctoral Research associate, The Jikei University School of Medicine, Tokyo, Japan, 2006-2008
Postdoctoral Research associate, University of Rochester School of Medicine and Dentistry, Rochester NY, 2008-2011

Board Certification

Medical Practitioner, National Medical Board in Japan, 2001
Medical License, Kanagawa Prefecture, Japan, 2001

University Appointment

Instructor

Research and Clinical Interests

My research interest is to understand the detail mechanism underlying the cardiac excitation and contraction/metabolism coupling by Ca2+ ion in the physiological and pathological conditions. I have a broad background in cardiac electrophysiology, with specific training and expertise. I am mainly investigating the significance of adrenergic signaling in heart and its regulation of cardiac ion channel/transporters using cardiac muscle cells.

My previous works were focusing on the regulation of cardiac ion channel/transporter by downstream kinases of adrenergic receptors especially PKA (Biochem Biophys Res Commun.2009, Circulation 2012), PKC, PKD (Circ Res 2012) and CaMKII (Proc Natl Acad Sci. USA, 2005, Circ Res, 2008, Am J Physiol Heart Circ Physiol. 2010). In addition, to acquire updated clinical information, I collaborated with clinical cardiologists in University of Rochester and investigated the risk stratification and therapy management for Long QT syndrome patients focusing on adrenergic modification of mutant human channels (Science Translational Medicine, 2011, Circulation 2012).

My current project is to determine the mitochondrial Ca2+ handling mechanisms in cardiac muscle cells under the guidance of Prof. Shey-Shing Sheu. Especially, I am interested in the functional modification of Ca2+ ion channel/transporters participating in mitochondrial Ca2+ influx mechanism by cardiac signaling in the physiological and pathological conditions.