ArticleExperimental physiology2022
NADPH oxidase 2 is necessary for chronic intermittent hypoxia-induced sternohyoid muscle weakness in adult male mice.
Article in Experimental physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles.International journal of molecular sciences · 2025Review
- Chronic Intermittent Hypoxia-Induced Diaphragm Muscle Weakness Is NADPH Oxidase-2 Dependent.Cells · 2023Article
- NADPH oxidase 2 is necessary for chronic intermittent hypoxia-induced sternohyoid muscle weakness in adult male mice.Experimental physiology · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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findingsWhat 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 sham and CIH-exposed NOX2-null mice (B6.129S-CybbTM
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