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Exosomal miR-107 antagonizes profibrotic phenotypes of pericytes by targeting a pathway involving HIF-1<b>α</b>/Notch1/PDGFR<b>β</b>/YAP1/Twist1 axis in vitro

Yi-Chun Wang, Han Xie, Yong-Chang Zhang, Qing-He Meng, Ming-Mei Xiong, Ming-Wang Jia, Fang Peng, Daolin Tang

2020American Journal of Physiology-Heart and Circulatory Physiology58 citationsDOI

Abstract

This work reveals a novel mechanism by which pulmonary vascular endothelial cells, via regulating the transdifferentiation of microvascular pericytes into myofibroblasts, contribute to the pathogenesis of pulmonary fibrosis. Since targeting the formation of myofibroblasts may prevent the development and benefit the treatment of pulmonary fibrosis, this study provides not only mechanistic understanding but also promising therapeutic targets for pulmonary fibrosis.

Topics & Concepts

TransdifferentiationMyofibroblastPulmonary fibrosisPhenotypeCancer researchPathogenesisFibrosisAngiogenesisYAP1PericyteMedicineIn vitroCell biologyBiologyPathologyEndothelial stem cellStem cellTranscription factorGeneticsGeneInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisExtracellular vesicles in diseasePulmonary Hypertension Research and Treatments
Exosomal miR-107 antagonizes profibrotic phenotypes of pericytes by targeting a pathway involving HIF-1<b>α</b>/Notch1/PDGFR<b>β</b>/YAP1/Twist1 axis in vitro | Litcius