The CRONIC-PPF Faculty

	Grażyna KWAPISZEWSKA Assoz. Prof. Priv.-Doz. Dr. Metabolic state of endothelial cells paves the way to lung fibrosis
Associate Professor, Otto Loewi Research Center; W3 Professor, Institute Lung Health, Justus Liebieg University, Giessen, Germany (partial position) Ludwig Boltzmann Institute for Lung Vascular Research, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz ✉ e-mail WWW: Forschungsportal Med Uni Graz ORCID: 0000-0003-0518-9079 PubMed: PubMed (nih.gov)
• Profile      • Curriculum vitae     • Publications

Grażyna Kwapiszewska is a molecular biologist with a strong research focus on the complex processes underlying vascular remodeling and the role of endothelial cells in pulmonary arterial hypertension (PAH) and pulmonary hypertension (PH)-ILD. Recently, she has characterized a specialized extracellular matrix, the basal membrane and its products (matrikines), in different forms of PH-ILD. She will contribute to this doc.funds with her know how of endothelial and smooth muscle cells, extracellular matrix and cellular signaling. She served as speaker of the doc.fund RESPImmun and is a vice-speaker of the Lung Research Cluster.

Project

Research interests

1. We have shown in series of studies that vascular component is involved in chronic lung diseases (CLD). We have performed first compartment specific transcriptomic studies on pulmonary arteries revealing underlying molecular differences in remodeled pulmonary arteries from different forms of CLD. By applying Fra-2 transgenic mouse model of systemic sclerosis, we documented that vascular remodeling proceeded parenchymal involvement and that skewing inflammation towards Th2 worsens the phenotype. (Birnhuber et al., 2025 [↗]; Fliesser et al., 2024 [↗]; Borek et al., 2023 [↗]; Fließer et al., 2023 [↗]; Hoffmann et al., 2014 [↗]; Seimetz et al., 2011 [↗]; Biasin et al., 2014 [↗]; Birnhuber et al., 2019 [↗]; Birnhuber et al., 2019 [↗]; Birnhuber et al., 2022 [↗])
2. Identified extensive changes in basement membrane components as potential breaking point in vascular homeostasis and crucial interaction point between EC and inflammatory cells. We have also established extensive and deep immune cell phenotyping of vascular compart and identified changes in rare inflammatory populations which might serve as a source of proteolytic enzymes leading to the remodeling processes. (Jandl et al., 2023 [↗]; Jandl et al., 2020 [↗]; Hoffmann et al., 2015 [↗]; Biasin et al., 2018 [↗]; Marsh et al., 2018 [↗]; Kwapiszewska et al., 2012 [↗])
3. Delineated the fate of major vascular resident cell populations in remodeling process showing distinct structural and compartment specific contribution of smooth muscle actin and PDGFRA-positive cells. We have also shown that lipid rich fibroblasts protect from the development of lung fibrosis. Finally, we have delineated the key role of cytoskeletal components in mediating smooth muscle cells proliferative response. (Crnkovic et al., 2015 [↗]; Lin et al., 2023 [↗]; Crnkovic et al., 2022 [↗]; Biasin et al., 2020 [↗]; Moiseenko et al., 2020 [↗]; El​Agha et al., 2017 [↗]; Kheirollahi et al., 2019 [↗]; Jandl et al., 2019 [↗]; Crnkovic et al., 2018 [↗]; Veith et al., 2014 [↗]; Veith et al., 2012 [↗]; Kwapiszewska et al., 2008 [↗])