{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSelenoprotein S (SELENOS) has emerged as a key mediator in endoplasmic reticulum (ER) protein quality control. Multiple studies demonstrate that SELENOS is up‐regulated in response to glucose deprivation and ER stress, where it participates in ER‐associated degradation by partnering with membrane proteins (e.g. Derlin‐1) and recruiting the cytosolic p97/VCP ATPase to retrotranslocate misfolded proteins. In doing so, SELENOS protects cells from oxidative stress and ER stress–induced apoptosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in protein quality control, SELENOS is intricately involved in the regulation of inflammation. Genetic variation in the SELENOS promoter influences its expression and has been linked to altered production of pro‐inflammatory cytokines such as interleukin‐6, interleukin‐1β, and tumor necrosis factor‐α. Functional studies have shown that both cytokine stimulation and ER stress increase SELENOS gene expression, suggesting that SELENOS forms part of a regulatory feedback loop moderating inflammatory responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSELENOS also plays a crucial role in metabolic regulation and adipocyte biology. Its expression in skeletal muscle and adipose tissues is modulated by insulin, with increased expression being associated with type 2 diabetes and insulin resistance. In adipocyte models, changes in SELENOS levels impact cell survival, differentiation, and the regulation of ER stress signaling pathways, thereby linking disturbances in SELENOS expression to metabolic dysregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the central nervous system, SELENOS is up‐regulated in reactive astrocytes upon brain injury and ER stress, where it has been shown to limit the expression of ER stress markers and pro‐inflammatory cytokines. This protective role extends to neurodegenerative processes; for example, increased SELENOS expression induced by selenium supplementation correlates with reduced hyperphosphorylation and aggregation of tau protein, implicating SELENOS as a factor that may mitigate Alzheimer’s disease pathology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its involvement in ER homeostasis and inflammation, SELENOS genetic variants are associated with risk for several cancers and autoimmune disorders. Polymorphisms in the SELENOS gene have been linked to altered susceptibility to colorectal and gastric cancers as well as autoimmune thyroid disease and rheumatoid arthritis. Such associations underscore the multifaceted role of SELENOS in cellular stress response pathways that may influence tumorigenesis and immune-mediated pathology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}, {"type": "fg_f", "ref": "11"}, {"type": "fg_fs", "start_ref": "23", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies reveal that SELENOS exerts influence over vascular and immune responses in diverse pathological contexts. Its genetic variants have been implicated in susceptibility to conditions such as ischemic stroke, sepsis, and even abnormal outcomes in premature birth. Moreover, SELENOS can be secreted from hepatocytes and has been shown to interact directly with viral proteins—such as the SARS‐CoV‑2 nonstructural protein 7—to potentially modulate viral replication complexes. Collectively, these findings highlight the multifunctional roles of SELENOS in modulating cellular responses during infection, inflammation, and systemic stress."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yuan Gao, Helen C Feng, Ken Walder, et al. 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