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
› Author Affiliations
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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