Overview

Dr. Quader's lab focuses on answering two central questions:

1. How to decrease reperfusion injury in Donation After Circulatory Death (DCD) donor hearts that have invariably sustained ischemic damage prior to procurement.
   
   
2. Establishing a viable ex vivo perfusion setup to keep the DCD hearts viable for an extended period.

Research

As a Professor of Cardiothoracic Surgery at Virginia Commonwealth University, I maintain an active clinical practice while also pursuing a focused interest in basic science research. I believe that the challenges faced daily in the operating room and in patient care are best investigated by the clinicians themselves in partnership with experts in complementary scientific disciplines. Rather than working in silos, I aim to bridge the clinical and research realms to produce knowledge that is both mechanistically sound and clinically translatable.

My research is rooted in the belief that scientific curiosity, clinical relevance, and technical rigor must intersect to drive meaningful innovation. My primary focus lies in the field of heart transplantation, particularly addressing ischemia-reperfusion injury in donation after circulatory death (DCD) hearts. Over the past decade, I have developed and refined small and large animal DCD models to simulate clinical conditions and explore interventions that mitigate myocardial injury, optimize perfusion, and improve post-transplant viability. My work centers on unraveling mitochondrial dysfunction, sterile inflammation, and temperature-flow dynamics—factors that critically influence DCD heart transplant outcomes. Below is a curated list of the key research questions I have pursued, each supported by peer-reviewed publications:

Research Questions and Supporting Publications

1. What is the optimal perfusion flow and temperature for DCD hearts?

Determination of Optimal Coronary Flow for the Preservation of "Donation after Circulatory Death" in Murine Heart Model.
Quader M, Toldo S, Torrado J, Mishra S, Mauro AG, Mezzaroma E, Heather R, Abbate A, Kasirajan V, Mangino M.
ASAIO J. 2018;64(2):225-231. [PMID: 28746080]

2. Do donor hearts stored in ice actually freeze?

Hypothermic Myocardial Preservation: The Freezing Debate. 
Quader M, Kiernan Z, Labate G, Chen Q. 
Transplant Proc. 2025;57(4):653-662. [PMID: 40087048] 

3. How does target temperature influence ex vivo perfusate selection?

Temperature and Flow Rate Limit the Optimal Ex-vivo Perfusion of the Heart – An Experimental Study. 
Quader M, Torrado JF, Mangino MJ, Toldo S.
J Cardiothorac Surg. 2020;15(1):180. [PMID: 32698846]

4. Can modulation of common inflammatory pathways diminish reperfusion injury in DCD hearts?

Targeting the NLRP3 Inflammasome to Reduce Warm Ischemic Injury in DCD Hearts.
Quader M, Mezzaroma E, Kenning K, Toldo S.
Clin Transplant. 2020;34(10):e14044. [PMID: 32654189]
 

5. How do ex vivo DCD ischemia models differ from in vivo DCD ischemia models?

Commonalities and Differences in Mitochondrial Dysfunction Between Ex Vivo and In Vivo Ischemia Models.
Quader M, Akande O, Toldo S, Cholyway R, Kang L, Lesnefsky EJ, Chen Q.
Front Physiol. 2020;11:681. [PMID: 32714203]

6. Is there a role for interleukin modulation post-perfusion in DCD hearts?

Modulation of IL-1 and IL-18 in DCD Mouse Hearts.
Quader M, Mezzaroma E, Kenning K, Toldo S..
J Surg Res. 2021;257:468-476. [PMID: 32896815]
 

7. What is the central role of mitochondria in DCD ischemia-reperfusion injury?

Ischemia and Reperfusion Injury to Mitochondria in DCD Hearts.
Akande O, Chen Q, Toldo S, Lesnefsky EJ, Quader M.
PLoS One. 2020;15(12):e0243504. [PMID: 33370296]
 

8. How can we reduce DCD injury by modulating mitochondrial respiration?

Modulation of Mitochondrial Respiration During Early Reperfusion in DCD Hearts.
Akande O, Chen Q, Cholyway R, Toldo S, Lesnefsky EJ, Quader M.
J Cardiovasc Pharmacol. 2022;80(1):148-157. [PMID: 35579563]

9. Can a murine heterotopic DCD heart transplant model be established?

A Heterotopic Rat Heart Transplantation Model Using Circulatory Death Donor Hearts.
Quader M, Cholyway R, Akande O, Bradley J, Mezzaroma E, Toldo S.
J Vis Exp. 2022;(183). [PMID: 35661103]

10. Can sterile inflammation inhibition improve function in heterotopic transplanted DCD heart?

Improving Circulatory Death Donor Heart Function: A Novel Approach.
Quader M, Mezzaroma E, Wickramaratne N, Toldo S.
JTCVS Tech. 2021;9:89-92. [PMID: 34647070]

11. What are the optimal machine perfusion conditions for DCD heart preservation?

Assessment of Machine Perfusion Conditions for DCD Hearts.
Cholyway R, Akande O, Mauro AG, Mezzaroma E, Wang R, Kenning K, Toldo S, Quader M.
Artif Organs. 2022;46(7):1346-1357. [PMID: 35167122]

12. How does gender influence ischemia-reperfusion tolerance in DCD rat hearts?

Influence of Sex on Myocardial Ischemia Tolerance and Mitochondrial Function.
Chen Q, Akande O, Lesnefsky EJ, Quader M.
Am J Physiol Heart Circ Physiol. 2023;324(1):H57-H66. [PMID: 36426883]

13. What is the role of Cyclosporine A in modulating mitochondrial permeability transition pores (MPTP) in DCD hearts?

Infarct Size With Incremental Ischemia Times: Cyclosporine A in DCD Rat Hearts.
Chen Q, Akande O, Lesnefsky EJ, Quader M.
Transplant Proc. 2023;55(7):1495-1503. [PMID: 37422374]

14. Can Cyclosporine A reduce infarct size in DCD hearts subjected to prolonged ischemia?

Infarct Size Reduction With Cyclosporine A in Circulatory Death Rat Hearts: Reducing Effective Ischemia Time With Therapy During Reperfusion.
Kiernan Z, Labate G, Chen Q, Lesnefsky EJ, Quader M.
Circ Heart Fail. 2024 (Online ahead of print). [PMID: 39301719] 

Lab Members

Contact Us

Mohammed Quader, MD
Professor
Cardiothoracic Surgery
School of Medicine Surgery
Virginia Commonwealth University
(e) mohammed.quader@vcuhealth.org
(p) 804-828-4641