Abstract
The endoplasmic reticulum (ER) is an important organelle for normal cellular function and homeostasis in most living things. ER stress, which impairs ER function, occurs when the ER is overwhelmed by newly introduced immature proteins or when calcium in the ER is depleted. A number of diseases are associated with ER stress, including otorhinolaryngological diseases. The relationship between ER stress and otorhinolaryngologic conditions has been the subject of investigation over the last decade. Among otologic diseases associated with ER stress are otitis media and hearing loss. In rhinologic diseases, chronic rhinosinusitis, allergic rhinitis, and obstructive sleep apnea are also significantly associated with ER stress. In this review, we provide a comprehensive overview of the relationship between ER stress and otorhinolaryngological diseases, focusing on the current state of knowledge and mechanisms that link ER stress and otorhinolaryngologic diseases.
Highlights
The endoplasmic reticulum (ER), a vesicle-like structure that branches out from the nuclear membrane, is categorized into two types: rough ER, containing ribosomes on its membrane surface, and smooth ER, which lacks ribosomes
ER stress causes the cell to engage in processes designed to overcome the resulting stress; these processes are mediated by three signaling systems: pancreatic ER kinase (PERK), inositol-requiring 1α (IRE-1α)/X-box binding protein 1 (XBP-1), and activating transcription factor 6 (ATF6) [1,2,5]
Cleaved caspase-9, caspase-3 and PARP1 were significantly increased in aged cochleae, suggesting that activation of apoptosis in the cochlea results from crosstalk between the ER and mitochondria through CHOP. These results indicate that impaired unfolded protein response (UPR) in cochleae of aged C57BL/6 mice and attendant ER stress may lead to apoptosis via the mitochondrial pathway and that ER stress-induced apoptosis may not be mediated by caspase-12 [48]
Summary
The endoplasmic reticulum (ER), a vesicle-like structure that branches out from the nuclear membrane, is categorized into two types: rough ER, containing ribosomes on its membrane surface, and smooth ER, which lacks ribosomes. Introduction of immature proteins to the extent that it exceeds the ER’s capacity, thereby overwhelming the ER and impairing its function, or depletion of calcium within the ER, results in a state called ER stress [3,4,5] These events induce a variety of cellular defense mechanisms that collectively serve to promote survival in a process called the ER stress response. Upper respiratory tract regions encompassing the ear, nose, and throat—the domain of the otorhinolaryngology field—are susceptible to various diseases, including infectious disease, ischemic disease, and cancer Given these shared vulnerabilities, the pathogenesis of various otorhinolaryngology-related diseases may be closely related to the ER stress response.
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