Open Access<p>Tranilast Inhibits Pulmonary Fibrosis by Suppressing TGFβ/SMAD2 Pathway</p>
Author(s) -
Motoyasu Kato,
Fumiyuki Takahashi,
Tadashi Satô,
Yoichiro Mitsuishi,
Ken Tajima,
Hiroaki Ihara,
Fariz Nurwidya,
Hario Baskoro,
Akiko Murakami,
Isao Kobayashi,
Moulid Hidayat,
Naoki Shimada,
Shinichi Sasaki,
Reiko Mineki,
Tsutomu Fujimura,
Takashi Kumasaka,
Shin-ichiro Niwa,
Kazuhisa Takahashi
Publication year - 2020
Publication title -
drug design, development and therapy
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s264715
Subject(s) - tranilast , fibronectin , pulmonary fibrosis , idiopathic pulmonary fibrosis , extracellular matrix , fibrosis , bleomycin , cancer research , medicine , transforming growth factor , chemistry , pharmacology , pathology , lung , biochemistry , chemotherapy
Idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of extracellular matrix (ECM) protein in the lungs. Transforming growth factor (TGF) β-induced ECM protein synthesis contributes to the development of IPF. Tranilast, an anti-allergy drug, suppresses TGFβ expression and inhibits interstitial renal fibrosis in animal models. However, the beneficial effects of tranilast or its mechanism as a therapy for pulmonary fibrosis have not been clarified.