Our mission is to identify and gain insights from the genetic and molecular pathways involved in cardiovascular disorders, and exploit these pathways to provide better therapeutic options to eradicate cardiovascular disease.
Our main objective is to broaden understanding of the cellular and molecular mechanisms involved in blood vessel wall patterning and define the role of these pathways in vascular abnormalities and complications, and then link these insights to translational research to improve the prevention and treatment of human cardiovascular disease.
To this end, we employ a unique blending of mouse models and cultured cells, as well as human samples, with the aim of unveiling the pathogenesis of cardiovascular diseases.
Our ultimate goal is to prevent and reverse vascular disease to prevent heart attack and stroke.
Cardiovascular disease is the main cause of death globally, accounting for approximately one third of all deaths. Currently available cardiovascular therapies are not universally effective and do not reverse the vascular disease completely. Vascular diseases therefore place a heavy burden on the health care system. Our work to identify the factors and signalling mechanisms involved in cardiovascular disorders has the potential to provide better options to treat and eradicate cardiovascular disease, thus decreasing its burden on society at large.
Tucker B, Kurup R, Barraclough J, Henriquez R, Cartland S, Arnott C, Misra A, Martínez G, Kavurma M, Patel S. Colchicine as a Novel Therapy for Suppressing Chemokine Production in Patients With an Acute Coronary Syndrome: A Pilot Study. Clin Ther. 2019 Oct;41(10):2172-2181. doi: 10.1016/j.clinthera.2019.07.015. Epub 2019 Aug 10. PubMed PMID: 31409556.
Bartlett B, Ludewick HP, Misra A, Lee S, Dwivedi G. Macrophages and T cells in atherosclerosis: a translational perspective. Am J Physiol Heart Circ Physiol. 2019 Aug 1;317(2):H375-H386. doi: 10.1152/ajpheart.00206.2019. Epub 2019 Jun 14. PubMed PMID: 31199186.
Misra A, et al. Integrin beta3 regulates clonality of smooth muscle-derived atherosclerotic plaque cells. Nature Communications, (2018), May 25;9(1):2073.