Education & Training
- Graduate School – University of Pittsburgh – PhD - Bioengineering
NIH Grants: T32
Dr. Shroff’s research interests are focused on three areas:
- Relationships between left ventricular mechano-energetic function and underlying cellular processes, with a special emphasis on contractile and regulatory proteins and post-translational regulation of cardiac contraction (e.g., via phosphorylation or acetylation). Whole heart, isolated muscle, and single cell experiments are performed using various animal models, including transgenic mice. Dr. Shroff and colleagues are currently using this basic information regarding structure-function relationships to develop novel inotropic therapies that are based on altering cellular composition using genetic means and to optimize the fabrication protocol for engineered cardiac tissue such that it possesses the desired contractile and energetic properties.
- The role of pulsatile arterial load (vascular stiffness in particular) in cardiovascular function and potential therapeutic applications of vascular and cardiac stiffness modifying drugs and/or hormones (e.g., relaxin). One of the hypotheses being investigated is that aberrant vascular stiffness changes are involved in the genesis of certain cardiovascular pathologies (e.g., preeclampsia, isolated systolic hypertension in elderly). In addition, relaxin’s therapeutic potential in the context of fibrosis-associated cardiac pathologies (e.g., atrial fibrillation, diastolic heart failure) is being investigated. Novel noninvasive measurement techniques are used to conduct longitudinal human studies, which are complemented by in vivo and in vitro vascular and cardiac studies with animal models.
- The role of regional contraction dyssynchrony in global ventricular mechanics and energetics. In addition to basic research, Dr. Shroff and colleagues have developed and continue to develop novel, simulation-based material (i.e., mathematical models of biological systems and associated "virtual experiments") for education and engineering design.
- Henry B, Gabris B, Li Q, Martin B, Parikh A, Patel D, Haney J, Schwartzman DS, Shroff SG, Salama G. Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na+ channels. Heart Rhythm 13: 983-981, 2016.
- Pinsky MR, Kim HK, Zenker S, Johnson L, Shroff SG. Differential effects of left ventricular pacing sites on regional contraction patterns and global performance. J. Cardiothorac. Vasc. Anesth. 30: 709-715, 2016.
- Samant SA, Pilai VB, Sundaresan NR, Shroff SG, Gupta MP. Histone Deacetylase 3 (HDAC3)-dependent reversible lysine acetylation of cardiac myosin heavy chain isoforms modulates their enzymatic and motor activity. J. Biol. Chem. 290:15559-15569, 2015.
- Parikh A, Patel DR, McTiernan CF, Xiang W, Haney J, Yang L, Lin B, Kaplan AD, Bett G, Rasmusson RL, Shroff SG, Schwartzman DS, Salama G. Relaxin suppresses atrial fibrillation by reversing fibrosis and myocyte hypertrophy, and increasing conduction velocity and sodium current in spontaneously hypertensive rat hearts. Circ Res 113:313-321, 2013.