[HTML][HTML] Lysyl hydroxylase inhibition by minoxidil blocks collagen deposition and prevents pulmonary fibrosis via TGF-β1/Smad3 signaling pathway

S Shao, X Zhang, L Duan, H Fang, S Rao… - … medical journal of …, 2018 - ncbi.nlm.nih.gov
S Shao, X Zhang, L Duan, H Fang, S Rao, W Liu, B Guo, X Zhang
Medical science monitor: international medical journal of experimental …, 2018ncbi.nlm.nih.gov
Background Idiopathic pulmonary fibrosis (IPF) is a deadly disease characterized by
excessive collagen in the extracellular matrix (ECM) of the lungs. Collagen is the primary
protein component of the ECM. However, the exact mechanisms underlying the formation
and deposition of collagen in the ECM under normal and pathological conditions remain
unclear. Previous studies showed that lysyl hydroxylase (LH) plays a crucial role in the
formation of collagen. Minoxidil is an FDA-approved anti-hypertensive agent that inhibits LH …
Abstract
Background
Idiopathic pulmonary fibrosis (IPF) is a deadly disease characterized by excessive collagen in the extracellular matrix (ECM) of the lungs. Collagen is the primary protein component of the ECM. However, the exact mechanisms underlying the formation and deposition of collagen in the ECM under normal and pathological conditions remain unclear. Previous studies showed that lysyl hydroxylase (LH) plays a crucial role in the formation of collagen. Minoxidil is an FDA-approved anti-hypertensive agent that inhibits LH that reduces fibrosis. In this study, we investigated the functional roles of LHs (LH1, LH2, and LH3) in pulmonary fibrosis and the anti-fibrotic effects of minoxidil.
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