The CRONIC-PPF Faculty

	Valentina BIASIN Priv.-Doz.in, MSc PhD Testosterone as a prognostic and mechanistic driver of sex differences in progressive pulmonary fibrosis
1st Deputy Speaker, Division of Physiology and Pathophysiology Otto Loewi Research Center, Division of Physiology and Pathophysiology, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz Phone: +43-316-385 72911, ✉ e-mail WWW: Forschungsportal Med Uni Graz ORCID: 0000-0002-6277-1463 PubMed: PubMed (nih.gov)
• Profile      • Curriculum vitae     • Publications

Valentina Biasin has studied molecular biotechnology and focuses on the cellular changes that occur in CLD, particularly how mesenchymal cells contribute to lung vascular and tissue remodelling in pulmonary arterial hypertension (PAH) and interstitial lung disease (ILD). Currently, her work explores the impact of sex hormones and metabolites on the phenotypic switching of mesenchymal cells.

Project

Research interests

1. PDGFRα‑positive fibroblasts as arbiters of repair versus fibrosis: Fibroblast heterogeneity shapes whether the injured lung heals or scars. Using integrated in vitro and in vivo models with advanced molecular profiling, we have on one hand identified PDGFRα‑positive fibroblasts as a fibroblast's population with pro‑fibrotic features but distinct lineage spatial niches from αSMA‑positive myofibroblasts. (Biasin et al., 2020 [↗])
   On the other hand, our results support the reparative capacity of PDGFRα⁺ fibroblasts where free fatty acid availability is a prerequisite enabling a switch from scarring to regeneration. (Unpublished data)
2. Metabolism and (sex) hormones as modifiers of tissue remodelling and fibrosis: Fibroblast activation is closely linked to metabolic rewiring. Our translational work has revealed that metabolic and hormonal alterations are critical nodes for modulating fibroblast behaviour and extracellular matrix (ECM) output. (Kheirollahi et al., 2019 [↗]; Bordag et al., 2025 [↗]; Muralikrishnan et al., 2025 [↗])
   Building on these findings, our ongoing studies indicate that testosterone exerts a pronounced influence in systemic sclerosis–associated interstitial lung disease (unpublished data). This suggests that androgen signaling intersects with fibroblast activation, ECM remodeling, and tissue repair capacity. Integrating (sex) hormones and metabolic pathways into our research framework may therefore enable the identification of tailored molecular targets and help account for sex-based differences in disease mechanisms and therapeutic responses.

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