TAK1 Inhibition Attenuates Both Inflammation and Fibrosis in Experimental Pneumoconiosis

Overview

Journal Cell Discov

Date 2017 Jul 13

PMID 28698801

Citations 23

Authors

Jie Li

Chao Liang

Zong-Kang Zhang

Xiaohua Pan

Songlin Peng

Wing-Sze Lee

Aiping Lu

Zhixiu Lin

Ge Zhang

Wing-Nang Leung

Bao-Ting Zhang

Affiliations

Soon will be listed here.

Abstract

Pneumoconiosis, caused by inhalation of mineral dusts, is a major occupational disease worldwide. Currently, there are no effective drugs owing to a lack of potential therapeutic targets during either the inflammation or fibrosis molecular events in pneumoconiosis. Here, we performed microarrays to identify aberrantly expressed genes in the above molecular events and found a hub gene transforming growth factor-β-activated kinase 1 (), which was highly expressed and activated in pneumoconiosis patients as well as silica-exposed rats with experimental pneumoconiosis. Genetic modulation of by CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9, RNA interference and overexpression indicated the important role of in both inflammation and fibrosis in experimental pneumoconiosis. To achieve pharmacological inhibition, we virtually screened out a natural product resveratrol, which targeted at both N161 and A107 residues, and significantly inhibited activation to attenuate inflammation and fibrosis . Consistently, prevention and intervention studies showed that resveratrol could inhibit pulmonary inflammation and fibrosis in silica-exposed rats.

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