Pneumologie 2025; 79(S 01): S109
DOI: 10.1055/s-0045-1804784
Abstracts
D2 – Grundlagen- und translationale Lungenforschung

PPAR-alpha Induction Inhibits TGF-b1- induced ROS Generation and Cell Proliferation in Lung IPF Fibroblasts

G Oruqaj
1   Medizinische Klinik Ii, Ukgm Giessen; Medizinische Klinik Ii, Pneumologie und Intensivmedizin; Pneumologie und Intensivmedizin
,
L Pervizaj-Oruqaj
2   Department of Internal Medicine V, Universities of Giessen and Marburg Lung Center, University Hospital Giessen, Justus Liebig University, Member of the German Center for Lung Research (Dzl), Giessen, Germany. – Gießen (Germany),; Ukgm Giessen; Department of Internal Medicine V
,
A Günther
3   Univ.-Klinikum Gießen; Med. Klinik Ii; Schwerpunkt Pneumologie
,
C Ruppert
4   Universities of Giessen & Marburg Lung Center (Ugmlc), Medizinische Klinik Ii, Justus-Liebig Universität Giessen; Deutsches Zentrum für Lungenforschung (Dzl)
,
N Sommer
5   Medizinische Klinik Ii, Exzellenz-Cluster Cardio-Pulmonary Institute (Cpi), Mitglied des Deutschen Zentrums für Lungenforschung (Dzl), Justus-Liebig-Universität Gießen; Universitätsklinikum Gießen
,
I Vadász
6   Universitätsklinikum Gießen und Marburg, Standort Gießen; Justus-Liebig-Universität Gießen; Medizinische Klinik Ii
,
K Tello
7   Universtitätklinik Gießen, Pneumologie; Medizinische Klinik Ii, Universitätsklinikum Gießen
,
M Hecker
8   Medizinische Klinik Ii
,
W Shi
9   University of Cincinnati College of Medicine; Com Im Pulmonary Division – 0564
,
S Herold
10   Universitätsklinikum Gießen; Justus-Liebig-Universität Gießen; Med. Klinik Ii
,
E Baumgart-Vogt
11   Justus Liebieg Universität, Institut für Anatomie und Zellbiologie; Medizinische Zellbiologie
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    The peroxisome proliferator-activated receptor-a (PPAR-α) has been an interesting target in different inflammation and fibrosis models in lung research. To evaluate the efficacy of PPAR-agonists, we used lung fibroblasts from both control subjects and IPF patients. PPAR-α significantly inhibited COL1A2 expression and reduced cellular injury following TGF-β1 treatment of IPF fibroblasts. Additionally, PPAR-α agonists significantly inhibited the IPF fibroblast proliferation and reactive oxygen species (ROS) generation in IPF fibroblasts, as well as TGF- β1 signaling pathway associated with proinflammatory and fibrotic responses. Therefore, we propose that the PPAR-α ligands alleviate inflammation, reduce ROS production, inhibit myofibroblast differentiation by modulating TGF-β signaling, potentially offering therapeutic benefits for limiting exacerbations and the progression of pulmonary fibrosis.


     

    Publication History

    Article published online:
    18 March 2025

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