Back to Journals » Journal of Inflammation Research » Volume 14

The Potentially Therapeutic Role of EPAC in Curbing the Process of Idiopathic Pulmonary Fibrosis via Differential Cellular Pathways

Authors Cao X, Li Y, Shi J, Tang H

Received 8 December 2020

Accepted for publication 27 January 2021

Published 26 February 2021 Volume 2021:14 Pages 611—619

DOI https://doi.org/10.2147/JIR.S296382

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Ning Quan


Xinwei Cao,1 Yajun Li,1 Jianrong Shi,2 Huifang Tang1

1Department of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, 310058, People’s Republic of China; 2Department of Clinical Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center For Child Health, Hangzhou, 310003, People’s Republic of China

Correspondence: Jianrong Shi
Department of Clinical Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center For Child Health, Hangzhou, People’s Republic of China
Email [email protected]
Huifang Tang
Department of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, People’s Republic of China
Email [email protected]

Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrosis disease caused by genetic susceptibility (causative) and other indirect risk factors such as smoking, micro-aspiration and air pollution. Repeated damage of lung epithelial cells can cause fibroblast activation and excessive collagen will lead the scar formation and severe fibrosis. It has been decades since drugs for the treatment of IPF were developed, but clinical choices were limited. Exchange Protein directly Activated by cAMP (EPAC), as a newly emerging cAMP (adenosine 3ʹ,5ʹ-cyclic monophosphate) downstream molecule, plays a vital role in the cellular pathways of IPF such as inhibiting fibroblast proliferation, stress fiber formation and epithelium cell adhesion, so it may be a novel target for drug development and treatment for curbing IPF. Here, we hypothesize that EPAC may participate in the signaling pathways related to IPF in different cell types (fibroblasts; airway smooth muscle cells; vascular endothelial cells; lung epithelial cells; macrophages; mesenchymal stem cells; T cells), thereby playing a potentially therapeutic role in resisting the process of fibrosis. We summarize the current correlation between EPAC and IPF in these different cell types, and further insights into EPAC will help to optimize the pharmacological treatment for IPF.

Keywords: EPAC, idiopathic pulmonary fibrosis, fibroblasts, cell types, cAMP, PKA

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]