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Endoplasmic reticulum stress and inflammation signaling in RPE cells
Author(s) -
SALMINEN A
Publication year - 2010
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2010.2233.x
Subject(s) - unfolded protein response , endoplasmic reticulum , atf6 , microbiology and biotechnology , inflammation , pathogenesis , signal transduction , biology , immunology , medicine
Pathogenesis of AMD is linked to augmentation of cellular stress, e.g. oxidative and proteotoxic stress, hypoxia and inflammation. All these conditions trigger stress in endoplasmic reticulum (ER) and in that way can disturb the protein quality control in retinal pigment epithelial (RPE) cells. ER stress stimulates the unfolded protein response (UPR) via the activation of IRE1, PERK and ATF6 transducers. The UPR signaling can restore cellular homeostasis but chronic and overwhelming stress can induce inflammatory response via different UPR signaling pathways and lead to apoptotic cell death. Moreover, ER stress is a well‐known inducer of vascular endothelial growth factor (VEGF) expression and in AMD, ER stress could provoke neovascularization and the conversion of dry form to wet counterpart. ER stress has a fundamental role in the pathogenesis of several diseases, e.g. in diabetes and neurodegenerative diseases. This lecture will review the recent advance in understanding the inducers of ER stress, present in RPE cells during AMD, and the possible role of ER stress in evoking inflammation and neovascularization during the pathogenesis of AMD.