Prem Prakash

Associate Professor

Cardiometabolic Therapeutics
Email: prem.prakash.cdri@gmail.com

Early detection of cardiometabolic conditions-including metabolic disorders and their cardiovascular complications-provides a window for effective intervention and potential cure. My research focuses on unravelling how damage-associated molecular patterns (DAMPs) drive inflammation and platelet activation in these conditions through Toll-like receptor 4 (TLR4) interactions, aiming to halt disease progression while it is still reversible.

We integrate small animal models of thrombosis, ischemia-reperfusion injury, stroke, cardiac hypertrophy, and platelet biology with artificial intelligence and in-silico strategies to identify therapeutic targets. Using intravital microscopy, we capture thrombosis in real-time to understand disease mechanisms dynamically. A key focus is discovering allosteric sites on TLR4, independent of the LPS binding site, to enable precise, side-effect-free therapies for cardiometabolic diseases.

Selected Recent Publications:

1. 1. Ali A, Gaba L, Jetley S, Khan IA, Prakash P, 2025. Neutrophil elastase binds at the central domain of extracellular Toll-like receptor 4: AI prediction, docking, and validation in disease model. Sci Rep. Mar 18;15(1):9282. doi: 10.1038/s41598-025-93511-6.
   
   
2. 2. Uzair M, Singhal C, Ali A, Rajak S, Kapoor A, Agarwal SK, Tiwari S, Pande S, Prakash P, 2024. Myocardial ischemia-reperfusion injury released cellular fibronectin-containing domain A (CFN-EDA): A destructive positive loop amplifying arterial thrombosis formation and exacerbating myocardial reperfusion injury. Thromb Res. Jun; 238:117-128.
   
   
3. 3. Gupta S, Ali A, Pandey S, Khan IA, Prakash P, 2022. Fibronectin containing alternatively spliced extra domain A interacts at the central and c-terminal domain of Toll-like receptor-4. Sci Rep., Jun 11, 12(1), 9662.
   
   
4. 4. Zhu W, Romano KA, Li L, Buffa JA, Sangwan N, Prakash P, Tittle AN, Li XS, Fu X, Androjna C, DiDonato AJ, Brinson K, Trapp BD, Fischbach MA, Rey FE, Hajjar AM, DiDonato JA, Hazen SL, 2021. Gut microbes impact stroke severity via the trimethylamine N-oxide pathway. Cell Host Microbe, 29, 1199-1208 e1195.
   
   
5. 5. Rajak S, Hussain Y, Singh K, Tiwari S, Ahmad B, Bharti S, Prakash P, 2020. Cellular fibronectin containing extra domain A causes insulin resistance via Toll-like Receptor 4. Sci Rep., Jun 4, 10(1), 9102.
   
   
6. 6. Chorawala MK, Prakash P, Doddapattar P, Jain M, Dhanesha N, Chauhan AK, 2018. Deletion of extra domain A of fibronectin reduces acute myocardial ischemia/reperfusion injury in hyperlipidemic mice by limiting thrombo-inflammation. ThrombHaemost., Aug, 118(8), 1450-1460.
   
   
7. 7. Misra A, Prakash P, Aggarwal H, Dhankani P, Kumar S, Pandey CP, Pugh N, Bihan D, Barthwal MK, Farndale RW, Dikshit DK, Dikshit M, 2018. Anti-thrombotic efficacy of S007-867: pre-clinical evaluation in experimental models of thrombosis in vivo and in vitro. BiochemPharmacol., Feb, 148, 288-297.
   
   
8. 8. Prakash P, Nayak MK, Chauhan AK 2016. P-selectin can promote thrombus propagation independently of both von Willebrand factor and thrombospondin1 in mice. J ThrombHaemost.,Feb, 15(2), 388-394.
   
   
9. 9. Prakash P, Kulkarni PP, Lentz SR, Chauhan AK, 2015. Cellular fibronectin containing extra domain A promotes arterial thrombosis in mice through platelet toll-like receptor 4. Blood, May 14, 125(20), 3164- 72.
   
   
10. 10. Prakash P, Kulkarni PP, Chauhan AK, 2015. Thrombospondin 1 requires von Willebrand factor to modulate arterial thrombosis in mice. Blood, Jan 8, 125(2), 399-406.