ArticleRespiratory physiology & neurobiology2015
Diaphragm dysfunction caused by sphingomyelinase requires the p47(phox) subunit of NADPH oxidase.
Article in Respiratory physiology & neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Redox Control of Skeletal Muscle Function and Adaptations to Exercise.Advances in experimental medicine and biology · 2025Review
- β2-Adrenergic Regulation of the Neuromuscular Transmission and Its Lipid-Dependent Switch.Molecular neurobiology · 2024Article
- Skeletal muscle redox signaling in rheumatoid arthritis.Clinical science (London, England : 1979) · 2020Review
- Keep Your Friends Close, but Your Enemies Closer: Role of Acid Sphingomyelinase During Infection and Host Response.Frontiers in medicine · 2020Review
- The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism.Antioxidants & redox signaling · 2019Review
- Small-hairpin RNA and pharmacological targeting of neutral sphingomyelinase prevent diaphragm weakness in rats with heart failure and reduced ejection fraction.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Muscle Weakness in Rheumatoid Arthritis: The Role of CaEBioMedicine · 2017Review
- Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology.Heart failure reviews · 2017Review
- Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016Review
- Diaphragm Abnormalities in Patients with End-Stage Heart Failure: NADPH Oxidase Upregulation and Protein Oxidation.Frontiers in physiology · 2016Article
- NAD(P)H oxidase subunit p47phox is elevated, and p47phox knockout prevents diaphragm contractile dysfunction in heart failure.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Sphingomyelinase (SMase) activity is elevated in inflammatory states and may contribute to muscle weakness in these conditions. Exogenous SMase depresses muscle force in an oxidant-dependent manner. However, the pathway stimulated by SMase that leads to muscle weakness is unclear. In non-muscle cells, SMase activates the Nox2 isoform of NADPH oxidase, which requires the p47(phox) subunit for enzyme function. We targeted p47(phox) genetically and pharmacologically (apocynin) to examine the role of NADPH oxidase on SMase-induced increase in oxidants and diaphragm weakness. SMase increased cytosolic oxidants (arbitrary units: control 203±15, SMase 276±22; P<0.05) and depressed maximal force in wild type mice (N/cm(2): control 20±1, SMase 16±0.6; P<0.05). However, p47(phox) deficient mice were protected from increased oxidants (arbitrary units: control 217±27, SMase 224±17) and loss of force elicited by SMase (N/cm(2): control 20±1, SMase 19±1). Apocynin appeared to partially prevent the decrease in force caused by SMase (n=3 mice/group). Thus, our study suggests that NADPH oxidase plays an important role on oxidant-mediated diaphragm weakness triggered by SMase. These observations provide further evidence that NADPH oxidase modulates skeletal muscle function.
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