@misc{Tkacz_Karolina_Molecular_2023,
 author={Tkacz, Karolina},
 address={Kraków},
 howpublished={online},
 year={2023},
 school={Rada Dyscypliny Nauki medyczne},
 language={pol},
 abstract={Myocarditis is a common cause of dilated cardiomyopathy characterized by fibrosis, ventricular stiffness, and heart failure. The pathophysiology of this disease involves many molecular pathways initiated by TGF-1\}, including the ROCK kinase-dependent pathway, as well as various cells, including fibroblasts and myofibroblasts differentiating in response to TGF-1\} and producing increased amounts of extracellular matrix proteins, leading to pathological changes in the structure and functioning of the heart. The developmen1 of dilated cardiomyopathy can be also regulate among others by the activity of monocytes and macrophages. The aim of this study was to investigate the role o1 ROCK kinases, as well as myofibroblasts and inflammatory macrophages in the development of postinflammatory dilated cardiomyopathy. The obtained results suggest that 1) ROCK kinases are not crucial in the development of autoimmune myocarditis and postinflammatory fibrosis 2) Myofibroblasts have a significant impact on the development of contractile dysfunction and cardiac hypertrophy, regardless of the degree of cardiac fibrosis 3) TGF-β signaling in inflammatory cardiac macrophages regulates the production of pro- and anti-inflammatory cytokines.},
 title={Molecular and cellular mechanisms in pathophysiology of post-inflammatory cardiac fibrosis},
 type={Praca doktorska},
 keywords={myocarditis, cardiac fibrosis, dilated cardiomyopathy, TGFβ, myofibroblasts},
}