Cardiovascular research

​Cardiovascular diseases (CVDs) affect the heart and blood vessels and are a leading cause of morbidity and mortality worldwide. They encompass a wide range of conditions including atherosclerosis, peripheral arterial disease, myocardial infarction (heart attack), and heart failure. Diabetic patients have a greater risk of developing CVD. Chronic kidney disease (CKD) is associated with a significantly increased risk of developing CVDs. Loss of coagulation regulators (thrombomodulin and activated protein C) have been repeatedly demonstrated CVDs and CKD. Thromboinflammation (interplay between the blood coagulation, and inflammatory responses) plays a significant role in the development and progression of various CVDs. Our work focuses on understanding the role of coagulation regulator and thromboinflammation in CVDs and CKD induced CVDs. Understanding the underlying mechanisms in CVDs will provide insights into potential therapeutic targets for the prevention and treatment of CVDs.

Our work is, or has been, funded by the German Research Council (DFG), European Foundation for the Study of Diabetes (EFSD), HELIOS Foundation, Foundation for Pathobiochemistry and Molecular Diagnostics (SPMD), and University of Leipzig.

Gadi I, Fatima S, Elwakiel A, Nazir S, Mohanad Al-Dabet M, Rana R, Bock F, Manoharan J, Gupta D, Biemann R, Nieswandt B, Braun-Dullaeus R, Besler C, Scholz M, Geffers R, Griffin JH, Esmon CT, Kohli S, Isermann B, Shahzad K. Different DOACs Control Inflammation in Cardiac Ischemia-Reperfusion Differently. Circ Res. 2021 Feb 19;128(4):513-529.

Nazir S, Gadi I, Al-Dabet MM, Elwakiel A, Kohli S, Ghosh S, Manoharan J, Ranjan S, Bock F, Braun-Dullaeus RC, Esmon CT, Huber TB, Camerer E, Dockendorff C, Griffin JH, Isermann B, Shahzad K. Cytoprotective activated protein C averts Nlrp3 inflammasome-induced ischemia-reperfusion injury via mTORC1 inhibition. Blood. 2017 Dec 14;130(24):2664-2677

Ambreen S, Fatima S, Elwakiel A, Rana R, Singh K, Gupta A, Gupta D, Khawaja H, Manoharan J, Besler C, Laufs U, Kohli S, Isermann B, Shahzad K. Hypercoagulability Impairs Plaque Stability in Diabetes-Induced Atherosclerosis. Nutrients. 2022 May 10;14(10):1991.

Shahzad K, Gadi, Nazir S, Al-Dabet MM, Kohli S, Bock F, Breitenstein L, Ranjan S, Fuchs T, Halloul Z, Nawroth PP, Pelicci PG, Braun-Dullaeus RC, Camerer E, Esmon CT, Isermann B. Activated protein C reverses epigenetically sustained p66Shc expression in plaque-associated macrophages in diabetes. Commun Biol. 2018 Aug 6;1:104

Seehaus S, Shahzad K, Kashif M, Vinnikov IA, Schiller M, Wang H, Madhusudhan T, Eckstein V, Bierhaus A, Bea F, Blessing E, Weiler H, Frommhold D, Nawroth PP, Isermann B. Hypercoagulability inhibits monocyte transendothelial migration through protease-activated receptor-1-, phospholipase-Cbeta-, phosphoinositide 3-kinase-, and nitric oxide-dependent signaling in monocytes and promotes plaque stability. Circulation 2009 Sep 1;120(9):774-84​

​Students interested in completing their thesis or practical work in our research group should please contact Dr. rer. nat. Khurrum Shahzad.