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