Pirfenidone and nintedanib attenuates pulmonary artery endothelial and smooth muscle cells transformations induced by IL-11

Nintedanib Pirfenidone Myofibroblast Neointima
DOI: 10.1016/j.ejphar.2024.176547 Publication Date: 2024-03-30T16:05:42Z
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) associated to hypertension (PH) portends a poor prognosis, characterized by lung parenchyma and artery remodeling. Serum levels of Interleukin 11 (IL-11) are elevated in IPF-PH patients contributes remodeling PH. However, the effect current approved therapies against IPF induced IL-11 is unknown. The aim this study analyze effects nintedanib pirfenidone on endothelial smooth muscle cell vitro. Our results show that (NTD) (PFD) ameliorates mesenchymal transition (EnMT), myofibroblast-like transformation precision cut slices. This provided also evidence inhibitory PFD NTD IL-11-induced cells proliferation senescence. these drugs monocyte arrest angiogenesis was studied. Finally, we observed canonical signal transducer activator transcription 3 (STAT3) non-canonical mitogen-activated protein kinase 1/2 (ERK1/2) phosphorylation, but, only inhibited ERK1/2 phosphorylation. Therefore, markers IL-11.
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