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Research Assistant Professor, Division of Hematology

Research Interests

My groups research is focused on identifying novel mechanisms responsible for pathological activation of coagulation and venous thromboembolism. Venous thromboembolism, including deep vein thrombosis and pulmonary embolism, is a common cardiovascular disease that is a major source of morbidity and mortality worldwide. The mechanisms that drive pathological activation of coagulation and venous thrombosis remain incompletely understood. We contend that a better understanding of these mechanisms will enable identification of at-risk populations and novel targets for the development of safe and effective anticoagulant drugs. A major focus of current efforts centers on the role of C1 inhibitor, a multifunctional serine protease inhibitor, as a negative regulator of pathological activation of coagulation. We have revealed novel associations between C1 inhibitor deficiency in humans, that causes the rare congenital swelling disorder Hereditary Angioedema, and increased contact pathway-mediated coagulation and risk of venous thromboembolism. Further, we have been able to model the procoagulant phenotype associated with Hereditary Angioedema in C1 inhibitor deficient mice. Additional research interests include evaluating the role of additional SERPINs and the complement factors in venous thrombosis.

Education and Experience

BSc: The University of Manchester, 2009

MRes: King’s College London, 2011

PhD: King’s College London, 2015

Postdoctoral Fellowship: Beth Israel Deaconess Medical Center & Harvard Medical School, 2015-2017

The University of North Carolina at Chapel Hill, 2017-2022

Research Assistant Professor: The University of North Carolina at Chapel Hill, 2022-Present

Selected Bibliography

Grover SP, Kawano T, Wan J, Tanratana P, Polai Z, Shim YJ, Snir O, Brækkan S, Dhrolia S, Kasthuri R, Bendapudi PK, McCrae KR, Wolberg AS, Hansen JB, Farkas H, Mackman N. C1 inhibitor deficiency enhances contact pathway mediated activation of coagulation and venous thrombosis. Blood. 2023: In Press.

Wan J, Tanratana P, Roest M, Gruber A, Pawlinski R, Wolberg AS, Mackman N, Grover SP. A novel mouse whole blood thrombin generation assay sensitive to FXI- and FIX-mediated amplification of coagulation. Blood Advances. 2022; In Press

Grover SP, Sundler Björkman L, Egesten A, Moll S, Mackman N. Hereditary angioedema is associated with an increased risk of venous thromboembolism. J Thromb Haemost. 2022; 20(11): 2703-2706

Grover SP, Olson TM, Cooley BC and Mackman N. Model-dependent contributions of FXII and FXI to venous thrombosis in mice. J Thromb Haemost. 2020;18(11):2899-2909.

Grover SP, Schmedes CM, Auriemma AC, Butler E, Parrish SL, Miszta A, Cleuren AC, Visser M, Heitmeier S, Posma JJ, Spronk HM, Antoniak S, Wolberg AS, Pawlinski R, Gailani D, Mackman N. Differential roles of factors IX and XI in murine hemostasis and placenta under conditions of low tissue factor. Blood Advances. 2020; 4(1): 207–216.

Full bibliography available here.

 

Website: www.thegroverlab.com

Steven Grover