RT Journal Article
T1 GLP-1 receptor agonist ameliorates experimental lung fibrosis
A1 Fandiño Gomez, Juan
A1 Toba Estévez, Laura
A1 González Matías, Lucas Carmelo
A1 Diz Chaves, Yolanda Maria
A1 Mallo Ferrer, Federico
K1 2410 Biología Humana
K1 2499 Otras Especialidades Biológicas
K1 32 Ciencias Médicas
K1 3205.08 Enfermedades Pulmonares
AB Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal lung disease. This disease is characterized by an excessive  accumulation of extracellular matrix deposition that modify normal lung physiology. Up to date, there are not efficient therapeutic tools to fight IPF. Glucagon-like peptide-1 receptor (GLP-1R) activation plays an  essential role in lung functions in normal and in pathological  conditions. The aim of the present study was to study the possible  beneficial effects of the administration of the GLP-1R agonist, liraglutide, in the pathogenesis of the fibrotic process in an animal model of pulmonary fibrosis induced by bleomycin. We observed that liraglutide decreased mRNA expression of collagen, hydroxyproline and key enzymes for the synthesis of collagen. In addition, GLP-1R activation restored the ACE2 mRNA levels modulating the activities of the RAS components, increased the production of surfactant proteins (SFTPa1, SFTPb, SFTPc) and promoted an improvement in pulmonary and cardiac functionality, including a partial restoration of lung alveolar structure. Liraglutide effects are shown at both the pro-inflammatory and fibrosis phases of the experimental disease. For these reasons, GLP-1 might be regarded as a promising drug for treating pulmonary fibrosis.
PB Scientific Reports
SN 20452322
YR 2020
FD 2020-10-22
LK http://hdl.handle.net/11093/2103
UL http://hdl.handle.net/11093/2103
LA eng
NO Scientific Reports, 10, 18091 (2020)
NO Xunta de Galicia | Ref. GPC2015/022
DS Investigo
RD 15-mar-2025