The CRONIC-PPF Faculty

	Paul W. VESELY (former STURM) Mag. Dr. rer. nat. Reprogramming epithelial metabolism to restore regenerative capacity in fibrotic lungs
Head of the Research Unit "Metabolism of Lung Regeneration" Otto Loewi Research Center, Lung Research Group, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz Phone: +43-316-385 72958, ✉ e-mail WWW: Forschungsportal Med Uni Graz ORCID: 0000-0003-3608-1060 PubMed: PubMed (nih.gov)
• Profile      • Curriculum vitae     • Publications

Paul W. Vesely is a molecular biologist with a research focus on metabolism of lung regeneration. He explores molecular mechanisms that abrogate epithelial repair and regeneration in COPD and interstitial pulmonary disease (IPF). He will contribute to CRONIC-PPF with his in-depth knowledge of the metabolic processes that are required to allow for successful lung epithelial regeneration.

Project

Research interests

1. In my corresponding author publication (Al-Zoughbi et al., Oncotarget 2016) we found that aged mice that are lacking the rate-limiting enzyme for lipolysis (ATGL) develop lung adenocarcinoma. This finding spawned our strong interest in the lung epithelial cell metabolism and its relevance for chronic lung disease. In my following corresponding author publication (Kanti et al., 2022 [↗]) we were the first to show that lipolysis driven peroxisome proliferator-activated receptor-α lipid-signaling is essential for lung airway epithelial regeneration. In my latest corresponding author publication (Peña de la Sancha et al., 2025 [↗]) we found that adipose tissue lipolysis regulates lipogenesis in peripheral tissue.
2. Several metabolic conditions, including central obesity, elevated blood triglyceride levels, hypertension and type-2 diabetes, are epidemiologically linked to reduced lung function and lung fibrosis. Idiopathic pulmonary fibrosis is a deadly disease. Patients suffer from restricted ventilation and insufficient gas exchange. Mean survival in untreated individuals is only 3 – 5 years and the two approved drugs pirfenidone and nintedanib may delay disease progression but do not heal it. Our unpublished data clearly show that functional lipolysis is essential for the lung-protective and regenerative functions of alveolar epithelial type II cells. We are convinced that pharmacological modification of cellular lipid signaling in the lungs holds great potential to reactivate the impaired regeneration potential in the alveolar epithelium of idiopathic pulmonary fibrosis patients.
3. Therefore, it is currently our main research interest to gain a better understanding of how lipolysis fuels lung epithelial repair. The gained knowledge will help the research community to develop potential disease modifying drugs against chronic lung diseases.

   05.04.2026 CRONIC-PPF · Doctoral Programme “Clinical & Research Oriented Network for Innovative Classification of Progressive Pulmonary Fibrosis”