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  Identification of novel inflammatory mechanisms as potential therapeutic targets in cardiovascular and metabolic diseases


   Department of Pharmacology and Pharmacotherapy

   Applications accepted all year round  Funded PhD Project (European/UK Students Only)

About the Project

The prognosis of chronic heart failure resulting from a heart attack is very poor, even with modern therapeutic devices and drugs, about half of the patients die within 5 years of diagnosis. The treatment of the disease puts a very heavy burden on the healthcare systems.

Heart failure can occur for many reasons, but during its development, the structure and functionality of the heart muscle is damaged. Despite the different etiology, cellular (neutrophil granulocytes, macrophages, B and T lymphocytes) and humoral inflammatory processes, inflammatory cytokines, neuropeptides such as IL-1β, IL-18 or TNF-α play an important role in the progression of heart failure, which significantly increase damage to the heart muscle. The aim of our studies is to investigate the therapeutic modulation of these cell types and different humoral factors both in acute myocardial infarction models and in pathological heart failure following the infarction.

After a heart attack, the damaged myocardium is flooded with inflammatory cells, which can contribute to heart damage (neutrophils participate in increased free radical formation) and chronic remodeling of the left ventricle (macrophages play a prominent role in fibrotic transformation). Normal myocardium can be seen on the left side of the histological diagram, next to it in the center is a large area of ​​infarcted myocardium, which is flooded with neutrophil granulocytes after the infarction. While on the right side, a section taken from the heart of a patient with chronic heart failure shows the appearance of macrophages

Acquired skills: histological techniques, immunohistochemistry, cell culture, fluorescent microscope management, RNA and protein work - Western blot, qRT-PCR

For further information or to register your interest please email

Biological Sciences (4) Medicine (26)

Funding Notes

Project no. RRF-2.3.1-21-2022-00003 has been implemented with the support provided by the European Union.


References

• Varga ZV, Pipicz M, Baán JA, Baranyai T, Koncsos G, Leszek P, Kuśmierczyk M, Sánchez-Cabo F, García-Pavía P, Brenner GJ, Giricz Z, Csont T, Mendler L, Lara-Pezzi E, Pacher P, Ferdinandy P. Alternative Splicing of NOX4 in the Failing Human Heart. Front Physiol. 2017 8:935. [IF: 3.394]
• Rajtik T, Goncalvesova E, Varga ZV, Leszek P, Kusmierczyk M, Hulman M, Kyselovic J, Ferdinandy P, Adameova A. Posttranslational modifications of calcium/calmodulin-dependent protein kinase IIδ and its downstream signaling in human failing hearts. Am J Transl Res. 20179:3573-3585. [IF: 3.061]
• Szobi A, Gonçalvesová E, Varga ZV, Leszek P, Kuśmierczyk M, Hulman M, Kyselovič J, Ferdinandy P, Adameová A. Analysis of necroptotic proteins in failing human hearts. J Transl Med. 2017 15:86. [IF: 4.197]
• Baán JA, Varga ZV, Leszek P, Kuśmierczyk M, Baranyai T, Dux L, Ferdinandy P, Braun T, Mendler L. Myostatin and IGF-I signaling in end-stage human heart failure: a qRT-PCR study. J Transl Med. 2015 16;13:1. [IF: 4.197]

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