The CRONIC-PPF Faculty

	Ákos HEINEMANN Univ.-Prof. Dr. med. univ. (MD) Succinate and its metabolites alter pro-fibrotic monocyte functions in progressive pulmonary fibrosis
Head of Division of Pharmacology of the Otto Loewi Research Center, Medical University of Graz Division of Pharmacology, Otto Loewi Research Centre, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz Phone: +43-316-385 74112, ✉ e-mail WWW: Forschungsportal Med Uni Graz ORCID: 0000-0002-8554-2372 PubMed: PubMed (nih.gov)
• Profile      • Curriculum vitae     • Publications

Ákos Heinemann is an established immunopharmacologist focusing on the regulation of leukocyte trafficking as a fundamental principle of tissue inflammation, particularly in the lung. He has characterized novel mediators and metabolic pathways that regulate the barrier function of the endothelium and its interaction with immune cells and elucidated their therapeutic potential in various disease models in the lung. Until recently he has been coordinating the doctoral programs MOLMED and was speaker of the FWF-funded doctoral college DK-MOLIN. Currently, his team is investigating the role of metabolic alterations and ER stress in the initiation and maintenance of lung fibrosis.

Project

Research interests

1. Technical development and clinical implementation of the basophil activation test (BAT) as a novel diagnostic tool in allergology, particularly in Hymenoptera venom allergies. (Sturm et al., 20095 [↗]; Bokanovic et al., 2013 [↗]; Sturm et al., 2004 [↗])
2. Characterization of prostaglandin D₂, its active metabolites and their receptors (CRTH2/DP D₂ and DP D₁) as novel targets in eosinophilic responses in allergic diseases and non-allergic inflammation. We described several novel small molecule antagonists of CRTH2 and their efficacy to inhibit eosinophil responses, have shown that that DP D₁ receptors are involved in eosinophil survival and migration and that both receptors are important signaling molecules in macrophages and innate lymphoid cells (ILC2). (Mathiesen et al., 2005 [↗]; Schratl et al., 2007 [↗]; Sedej et al., 2012 [↗]; Schmidt et al., 2013 [↗]; Jandl et al., 2016 [↗]; Maric et al., 2019 [↗])
3. Protective role of EP₄ receptors in lung pathologies. We could delineate the protective effects of prostaglandin E₂ in the lung as a bundle of mechanisms in different cell types mediated by the G-protein-coupled receptor EP₄. Activation of EP₄ receptors attenuates eosinophil recruitment and activation, ILC2 activity, and cytokine secretion, but strengthens the endothelial barrier. Deposition of collagen, proliferation of myofibroblasts and recruitment of fibrocytes is likewise reversed by blockade of PGE₂ metabolism. We observed corresponding beneficial effects in mouse models of allergic airway inflammation, acute lung injury and lung fibrosis. (Bärnthaler et al., 2020 [↗]; Maric et al., 2018 [↗]; Luschnig-Schratl et al., 2011 [↗]; Jandl et al., 2016 [↗]; Konya et al., 2013 [↗]; Sturm et al., 2008 [↗])

03.04.2026 CRONIC-PPF · Doctoral Programme “Clinical & Research Oriented Network for Innovative Classification of Progressive Pulmonary Fibrosis”