Endoplasmic reticulum stress and bronchial asthma
CSTR:
Author:
Affiliation:

Department of Respiratory Medicine, Changhai Hospital, Second Military Medical University,Department of Respiratory Medicine, Changhai Hospital,Second Military Medical University

Clc Number:

Fund Project:

Supported by National Natural Science Foundation of China(81000006) and Shanghai Pujiang Talent Program (14PJ1411000).

  • Article
  • |
  • Figures
  • |
  • Metrics
  • |
  • Reference
  • |
  • Related
  • |
  • Cited by
  • |
  • Materials
  • |
  • Comments
    Abstract:

    The endoplasmic reticulum stress (ERS) response is induced by misfolded proteins via the unfolded-protein response (UPR),allowing cells to deal with endogenous stress through arresting of protein translation,promoting peptide folding,degeneration of unfolded or misshapen proteins,and cell apoptosis.Pancreatic endoplasmic reticulum kinase (PERK),inositol-requiring transmembrane kinase/endonuclease 1 (IRE1) and activating transcription factor 6 (ATF6) are the three proximal effectors of the UPR in mammalian cells.Airway epithelial cells consist of many cell types with prosperous cell growth and numerous secretion,making those cells more liable to have ERS.Recent studies have revealed the role of ERS in the pathogenesis of bronchial asthma,which involves imbalance of calcium homeostasis,abnormal secretion of hyaluronic acid and mucin,and the abnormal recruitment and infiltration of inflammatory cells.This article summarizes the correlation of ERS with asthma.

    Reference
    Related
    Cited by
Related Videos

Share
Article Metrics
  • Abstract:
  • PDF:
  • HTML:
  • Cited by:
History
  • Received:May 11,2014
  • Revised:August 25,2014
  • Adopted:July 08,2014
  • Online: January 21,2015
  • Published:
Article QR Code