Staff Physician and Associate Chief of Medicine for Research, SFVAMC
Professor of Medicine and Cardiology, UCSF

Email: joel.karliner@va.gov

Dr. Karliner uses models of heart disease in rodents to study the effects of drugs and of the body's natural defenses, with the goal of understanding how these drugs and defenses might be used to prevent acute heart attacks. These models simulate acute heart attack through either oxygen deprivation or abrupt cessation of blood supply to the heart in order to determine the functional and biochemical effects of these interventions. Effects of drugs and natural defenses are investigated in heart tissue, isolated heart cells, and mitochondria, which generate energy within cells. These studies also include the use of genetically altered mice in which one gene is deleted or excessively active, in order to discover how these genes and the proteins that are derived from them are involved in the mechanisms of protection against heart attack. New knowledge about the mechanism of action of these drugs and defenses, and how they affect biochemical signals and enzymes, can lead to new strategies that would either prevent or ameliorate heart damage in patients undergoing a variety of procedures. These procedures include both cardiac and noncardiac surgery in patients, especially elderly veterans, who are at higher risk for heart damage during and after stressful procedures. Patients undergoing stent deployment in coronary arteries and other vessels will also benefit.

Jin ZQ, Zhang J, Huang Y, Hoover HE, Vessey DA, Karliner JS. 2007. A sphingosine kinase 1 mutation sensitizes the myocardium to ischemia/reperfusion injury. Cardiovasc Res 76:41-50. 

Vessey DA, Li L, Kelley M, Karliner JS. 2008. Combined sphingosine, S1P and ischemic postconditioning rescue the heart after protracted ischemia. Biochem Biophys Res Commun 375:425-429.