Nora Eccles Harrison Cardiovascular Research & Training Institute

The Drakos Laboratory

The Drakos Lab Cardiovascular Research Team at CVRTI Fall BBQ
CVRTI Drakos Lab University of Utah Health Care
CVRTI Heart Graphic with Charts and Cardiograph Lines

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

The Pyruvate-Lactate Axis Modulates Cardiac Hypertrophy and Heart Failure. 
https://www.sciencedirect.com/science/article/pii/S1550413120306586

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.
https://doi.org/10.1161/CIRCULATIONAHA.119.044452

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

https://www.nature.com/articles/s41467-021-24869-0

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
Professor

Jing Ling
Sr. Lab Specialist/Lab Manager

Sutip Navankasattusas, PhD
Sr. Research Associate

Joe Visker, PhD
Postdoctoral Fellow

Christos Kyriakopoulos, MD
Postdoctoral Fellow

Anu Shankar, PhD
Graduate Student

Eleni Tseliou,MD,PhD

Physician Scientist Training Track

Dallen Calder
Undergraduate Student

Sophia Skedros
Undergraduate student

Iosif Taleb, MD
Post Doctoral Fellow

Elizabeth Lynn Stauder
Medical Student

Kimiya Nourian
Medical Student