The CRONIC-PPF Faculty

	Thomas BÄRNTHALER Ass.-Prof. Priv.-Doz. Dr.med.univ. PhD Peripheral blood signatures of antifibrotics in patients with progressive pulmonary fibrosis
Head of Research Unit "Molecular Pharmacology in Pulmonary Diseases" Division of Pharmacology, Otto Loewi Research Centre, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz Phone: +43-316-385 74106, ✉ e-mail WWW: Forschungsportal Med Uni Graz ORCID: 0000-0002-4988-3700 PubMed: PubMed (nih.gov)
• Profile      • Curriculum vitae     • Publications

Thomas Bärnthaler is a physician-scientist in the field of pharmacology focusing on therapeutic targets in pulmonary fibrosis. Recently, he showed that inhibition of 15-prostaglandin dehydrogenase, the PGE₂-degrading enzyme, increases PGE₂ levels in the lungs and thereby might represent a novel therapeutic target in fibrotic lung disease. Currently, he is investigating the antifibrotic mechanism of treprostinil and its effects on different cell types.

Project

Research interests

1. Pulmonary fibrosis, idiopathic pulmonary fibrosis, prostaglandins, lung physiology. The most important results so far are represented by contributions to our understanding of pulmonary physiology and pathology with a focus on pulmonary fibrosis. A part of the work investigated prostaglandins and related lipid mediators in the lung and how these can be targeted.
2. In a first step, we could show that prostaglandin E₂ mediates interaction between different pulmonary cell types. However, as this molecule is rapidly degraded in vivo, we investigated approaches to indirectly modulates its levels, leading to the discovery that imatinib, a tyrosinkinase inhibitor, used for the treatment for chronic myeloic leukemia, can increase PGE₂ synthesis, thereby exerting anti-inflammatory effects.
3. In a subsequent work, we could show that inhibition of 15-prostaglandin dehydrogenase, the PGE₂-degrading enzyme, increases PGE₂ levels in the lungs and thereby might represent a novel therapeutic target in fibrotic lung disease. This work ties well into my focus on pulmonary disease and especially pulmonary fibrosis. I joined Nafatli Kaminski’s lab as a postdoc where I could contribute to the discovery and preclinical validation of a promising novel therapeutic agent for IPF, saracatinib, predicted by computational workflows. Upon my return, I established a research group focused on new therapies for pulmonary fibrosis (2 PhD students, 1 post-doc, 1 technician).

   04.04.2026 CRONIC-PPF · Doctoral Programme “Clinical & Research Oriented Network for Innovative Classification of Progressive Pulmonary Fibrosis”