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This publication is protected and can be accessed only from certain IPs.

Title: Molecular and cellular mechanisms in pathophysiology of post-inflammatory cardiac fibrosis

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.

Place of publishing:

Kraków

Level of degree:

2 - studia doktoranckie

Degree grantor:

Rada Dyscypliny Nauki medyczne

Promoter:

Błyszczuk, Przemysław

Date issued:

2023

Identifier:

oai:dl.cm-uj.krakow.pl:5179

Call number:

ZB-141570

Language:

pol

Access rights:

tylko w bibliotece

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Last modified:

Dec 30, 2024

In our library since:

Dec 30, 2024

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3

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0

All available object's versions:

http://dl.cm-uj.krakow.pl:8080/publication/5180

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ZB-141570 Dec 30, 2024
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