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.
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
The Role of Nonglycolytic Glucose Metabolism in Myocardial Recovery Upon Mechanical Unloading and Circulatory Support in Chronic Heart Failure Circulation.
Based on the findings of the aforementioned study (#1) we hypothesized that the accumulated glycolytic intermediates are channeled into accessory pathways of glucose metabolism that are cardioprotective and may induce myocardial recover.
Badolia R, Ramadurai DKA, Abel ED, Ferrin P, Taleb I, Shankar TS, Navankasattusas S, Wever-Pinzon O, Selzman CH, Chaudhuri D, Rutter J, Drakos SG. The Role of Nonglycolytic Glucose Metabolism in Myocardial Recovery Upon Mechanical Unloading and Circulatory Support in Chronic Heart Failure Circulation. 2020;142(3):259-274.
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
Sutip Navankasattusas, PhD
Joe Visker, PhD
Christos P. Kyriakopoulos,MD
Anu Shankar, PhD
Physician Scientist Training Track
Iosif Taleb, MD
Elizabeth Lynn Stauder