The Drakos Laboratory
The Drakos Laboratory’s research is focused on cardiac recovery associated with unloading and mechanical circulatory support (MCS) in the chronic heart failure (HF) setting and the acute setting (i.e. acute HF/cardiogenic shock). We have published original work generated both in the clinical arena and in our laboratory which led to the founding and establishment of the award-winning multidisciplinary Utah Cardiac Recovery Program (UCAR). The research initiatives of UCAR are developed in close connection and alignment to the development of its clinical aspects. This parallel development facilitates a full circle bidirectional synergy which is mutually beneficial to the research and clinical potentials.
Featured Publications
 | Enhancing mitochondrial pyruvate metabolism ameliorates ischemic reperfusion injury in the heart | We investigated a pharmacological approach of MCT4 inhibition to boost pyruvate metabolism and reduce the damage after a heart attack, which is a leading cause of death worldwide and a primary cause of heart failure. | Visker JR, Cluntun AC, Velasco-Silva JN, Eberhardt DR, Cedeno-Rosario L, Shankar TS, Hamouche R, Ling J, Kwak H, Hillas JY, Aist I, Tseliou E, Navankasattusas S, Chaudhuri D, Ducker GS, Drakos SG, Rutter J |
 | The Pyruvate-Lactate Axis Modulates Cardiac Hypertrophy and Heart Failure. | Myocardial MPC expression coincides with LVAD-mediated recovery in chronic HF patients. Loss of the MPC in cultured cells and in murine hearts is sufficient to induce hypertrophy and HF. MPC overexpression attenuates drug-induced hypertrophy in a cell-autonomous manner. Inhibition of MCT4 can mitigate hypertrophy in cultured cardiomyocyte and in mice. | Cluntun AC*, Badolia R* (co-first authors), Lettlova S, Parnell KM, Shankar T, Diakos NA, Olson KA, Taleb I, Tatum SM, Berg JA, Cunningham CN, Van Ry T, Bott AJ, Thodou A, Fogarty S, Skedros S, Swiatek WI, Yu X, Luo B, Merx S, Navankasattusas S, Cox JE, Ducker GS, Holland WL, McKellar SH, Rutter J, Drakos SG. The Pyruvate-Lactate Axis Modulates Cardiac Hypertrophy and Heart Failure. Cell Metabolism, In Press |
 | Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis | our findings demonstrate that VDAC2 plays a crucial role in cardiac function by influencing cellular calcium signaling. Through this unique role in cellular calcium dynamics and excitation-contraction coupling VDAC2 emerges as a plausible therapeutic target for heart failure. | Shankar TS, Ramadurai DKA, Steinhorst K, Sommakia S, Badolia R, Krokidi AT, Calder D, Sander P, Kwon OS, Ling J, Dendorfer A, Xie C, Kwon O, Cheng EHY, Whitehead KJ, Richardson RS, Sachse FB, Schredelseker J, Spitzer KW, Chaudhuri D, Drakos SG. Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis. Nature Communications, In Press |
The Drakos Lab Research Team
 Stavros Drakos, MD, PhD |  Jing Ling |  Sutip Navankasattusas, PhD |
 Joe Visker, PhD |  Christos P. Kyriakopoulos,MD Postdoctoral Fellow |  Anu Shankar, PhD |
 Eleni Tseliou,MD,PhD Physician Scientist Training Track |  Dallen Calder |  Sophia Skedros |
 Iosif Taleb, MD |  Elizabeth Lynn Stauder |  Kimiya Nourian |
