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. 2022 Apr 26;13:879204. doi: 10.3389/fphar.2022.879204

FIGURE 2.

FIGURE 2

ER stress in pulmonary disease. Pulmonary pathologies, including pulmonary fibrosis, pulmonary infection, asthma, Chronic obstructive pulmonary disease and lung cancer lead to endoplasmic reticulum (ER) stress and induce the unfolded protein response (UPR) (which has three branches, mediated by protein kinase RNA-like ER kinase (PERK), Inositol-requiring protein 1α (IRE1α) and activating factor 6 (ATF6) to tackle ER stress. However, if the UPR fails to restore ER homeostasis, it might induce risk factors for pulmonary disease, including increased reactive oxygen species (ROS) production, inflammation, and apoptosis, which further aggravate pulmonary disease. BAX, BCL-2-associated X protein; CHOP, C/EBP homologous protein; ERAD, ER-associated degradation; JNK1, JUN N-terminal kinase 1; The NK-kappa B, nuclear factor kappa B predominate; NLRP3, NACHT, LRR and PYD domains-containing protein 3; NADPH, nicotinamide adenine dinucleotide phosphate; NRF2, nuclear factor erythroid 2-related factor 2; REDD1, protein regulated in development and DNA damage response 1; TRAF2, TNF receptor associated factor 2; XBP1s, spliced X-box-binding protein 1.