Table 1

Therapeutic intervention of UPR and ER stress

Therapeutic agentDiseaseExperimental modelReferences
SalubrinalCOPD, asthmaIn vitro (HBE, COPD HBE, BEAS-2B, HEK cells); in vivo (murine, ferret) 73 75 91 92
mTOR inhibitor (rapamycin)In vitro (MEF cells) 93
AMPK activators (metformin)Diabetes, metabolic diseasesIn vivo (murine) 94
PPAR agonistsMetabolic diseasesIn vitro (HepG2); in vivo (murine) 94
PERK and IRE1 inhibitorsCancerIn vitro (C6 cells) 94
Chemical chaperones (4-PBA,TUDCA)Pulmonary fibrosis, asthmaIn vivo (murine); ex vivo (BALF) 67 68 95–97
  • BALF, bronchoalveolar lavage fluid; BEAS-2B, bronchial epithelial cell line; C6, glioma cell line; ER, endoplasmic reticulum; HBE, primary human bronchial epithelial cells; HEK, human embryonic kidney; HepG2, liver hepatocellular carcinoma cell line; IRE, inositol-requiring enzyme; MEF, mouse embryonic fibroblasts; mTOR, mammalian target of rapamycin; PBA, phenylbutryic acid; PPAR, peroxisome proliferator-activated receptor; TUDCA, tauroursodeoxycholic acid; UPR, unfolded protein response.