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NADPH oxidase 2 is necessary for chronic intermittent hypoxia‐induced sternohyoid muscle weakness in adult male mice by Sarah E. Drummond; David P. Burns; Sarah El Maghrani; Oscar Ziegler; Vincent Healy; Ken D. O'Halloran is a Medicine article available to read on EtoBox.

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## New Findings What is the central question of this study? Exposure to chronic intermittent hypoxia (CIH) evokes redox changes, culminating in impaired upper airway muscle function: what is the specific source of CIH‐induced reactive oxygen species? What is the main finding and its importance? Profound sternohyoid muscle dysfunction following exposure to CIH was entirely prevented by apocynin co‐treatment or NADPH oxidase 2 (NOX2) deletion. The results have implications for human obstructive sleep apnoea syndrome and point to antioxidant intervention, potentially targeting NOX2 blockade, as a therapeutic strategy. ## Abstract Exposure to chronic intermittent hypoxia (CIH) evokes redox changes, culminating in impaired upper airway muscle function. We sought to determine if NADPH oxidase 2 (NOX2)‐derived reactive oxygen species underpin CIH‐induced maladaptive changes in upper airway (sternohyoid) muscle performance. Adult male mice (C57BL/6J) were assigned to one of three groups: normoxic controls (sham); CIH‐exposed (CIH, 12 cycles/hour, 8 h/day for 14 days); and CIH + apocynin (NOX2 inhibitor, 2 mM) given in the drinking water throughout exposure to CIH. In addition, we studied s

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Author
Sarah E. Drummond; David P. Burns; Sarah El Maghrani; Oscar Ziegler; Vincent Healy; Ken D. O'Halloran
Publisher
Wiley
Published
2022
Language
EN
Field
Medicine (Health Sciences)

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