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Md Nasimuzzaman, PhD

  • Member, Division of Experimental Hematology & Cancer Biology
  • Instructor, UC Department of Pediatrics



The primary objective of my research is to define the mechanisms by which coagulation system activity, including hyperactivation of coagulation proteases, exacerbates sickle cell anemia (SCA) pathogenesis. I am particularly interested in dissecting the role of the thrombin-protease-activated receptor (PAR) signaling in organ dysfunctions and pathologies of SCA using mouse models.

I am developing my independent research program to become an extramurally funded investigator in the field of coagulation-mediated pathogenesis of SCA. I expect my proposed studies will serve to highlight novel possibilities for pharmaceutical intervention to fill a much-needed clinical gap for SCA.

SCA affects over 100,000 Americans and more than 20 million individuals worldwide. The disease costs approximately $1.2 billion every year in healthcare costs in the United States alone. It causes hemolytic anemia, recurrent vaso-occlusion, inflammation, and cumulative multi-organ damage leading to premature death. However, SCA patients are now surviving through adulthood due to newborn screening, prophylaxis and improved comprehensive medical care in the developed world.

These approaches have changed the disease manifestations. Nowadays, organ pathologies have emerged as the most common cause of death in SCA. Current therapeutic options are limited to chronic transfusions, hydroxyurea and bone marrow transplants. However, these therapies are unfortunately associated with toxicity in some patients, and they have limited availability in the underdeveloped and developing world.

Novel therapies that ameliorate disease phenotype and reduce organ damage are urgently needed for this devastating disease. I hope my research will help contribute to the development of new treatments for people living with SCA.

Throughout my research career, I have received several notable honors and awards, including:

  • 1992 University of Dhaka Merit Scholarship for BS studies
  • 1997 University of Dhaka Merit Scholarship for MS studies
  • 1998 Japan Government Scholarship
  • 2003 Kochi University President’s Award for the Best Young Researcher
  • 2004 Japan Society for the Promotion of Science (JSPS) Fellowship
  • 2005 American Society for Microbiology (ASM) Travel Grant Award
  • 2008 American Society of Virology (ASV) Travel Grant Award
  • 2011 American Society of Gene and Cell Therapy (ASGCT) Travel Grant Award
  • 2015 ASGCT Outstanding Research Award
  • 2016 Sickle Cell Disease Research Scholar
  • 2018 University of Cincinnati Pilot Translational Award
  • 2020 University of Cincinnati Just-in Time Award


A mutant fibrinogen that is unable to form fibrin can improve renal phenotype in mice with sickle cell anemia. Narciso, MG; Hoeting, B; James, JM; VandenHeuvel, K; Nasimuzzaman, M. 2021; 2:462-465.

Purification Platelets from Mouse Blood with Sickle Cell Disease Using Iohexol Gradient Medium. Nasimuzzaman, M. Blood. 2019; 134:4888-4888.

Role of the coagulation system in the pathogenesis of sickle cell disease. Nasimuzzaman, M; Malik, P. Blood Advances. 2019; 3:3170-3180.

Elimination of the fibrinogen integrin αMβ2-binding motif improves renal pathology in mice with sickle cell anemia. Nasimuzzaman, M; Arumugam, PI; Mullins, ES; James, JM; VandenHeuvel, K; Narciso, MG; Shaw, MA; McGraw, S; Aronow, BJ; Malik, P. Blood Advances. 2019; 3:1519-1532.

Purification of Platelets from Mouse Blood. Narciso, MG; Nasimuzzaman, M. Journal of Visualized Experiments. 2019.

Production and Purification of Baculovirus for Gene Therapy Application. Nasimuzzaman, M; van der Loo, JC M; Malik, P. Journal of Visualized Experiments. 2018.

Foamy Virus Vector Carries a Strong Insulator in Its Long Terminal Repeat Which Reduces Its Genotoxic Potential. Goodman, MA; Arumugam, P; Pillis, DM; Loberg, A; Nasimuzzaman, M; Lynn, D; van der Loo, JC M; Dexheimer, PJ; Keddache, M; Jr, BT R; et al. Journal of Virology. 2018; 92.