ArticleJournal of applied physiology (Bethesda, Md. : 1985)2015
Diaphragm muscle weakness in mice is early-onset post-myocardial infarction and associated with elevated protein oxidation.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Post-Myocardial Infarction Rehabilitation: The Absence in the Rehabilitation Process of the Diaphragm Muscle.International journal of general medicine · 2024Review
- Skeletal muscle atrophy, regeneration, and dysfunction in heart failure: Impact of exercise training.Journal of sport and health science · 2023Review
- Chronic Intermittent Hypoxia-Induced Diaphragm Muscle Weakness Is NADPH Oxidase-2 Dependent.Cells · 2023Article
- The Importance of Diaphragmatic Function in Neuromuscular Expression in Patients With Chronic Heart Failure.Cureus · 2023Review
- Skeletal muscle Nox4 knockout prevents and Nox2 knockout blunts loss of maximal diaphragm force in mice with heart failure with reduced ejection fraction.Free radical biology & medicine · 2023Article
- Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023Review
- NADPH oxidase 2 is necessary for chronic intermittent hypoxia-induced sternohyoid muscle weakness in adult male mice.Experimental physiology · 2022Article
- Differential Regulation of Myocardial E3 Ligases and Deubiquitinases in Ischemic Heart Failure.Life (Basel, Switzerland) · 2021Article
- Nox4 Knockout Does Not Prevent Diaphragm Atrophy, Contractile Dysfunction, or Mitochondrial Maladaptation in the Early Phase Post-Myocardial Infarction in Mice.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- Article
- Redox Control of Proteolysis During Inactivity-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2020Review
- Cardiac Rehab for Functional Improvement.Current heart failure reports · 2020Review
- Article
- Skeletal myofiber VEGF deficiency leads to mitochondrial, structural, and contractile alterations in mouse diaphragm.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Mitochondrial respiration and HAmerican journal of physiology. Cell physiology · 2019Article
- Small-molecule-mediated chemical knock-down of MuRF1/MuRF2 and attenuation of diaphragm dysfunction in chronic heart failure.Journal of cachexia, sarcopenia and muscle · 2019Article
- Exercise in Heart Failure-What Is the Optimal Dose to Improve Pathophysiology and Exercise Capacity?Current heart failure reports · 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
- Oxidative hotspots on actin promote skeletal muscle weakness in rheumatoid arthritis.JCI insight · 2019Article
- Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure induced by myocardial infarction (MI) causes diaphragm muscle weakness, with elevated oxidants implicated. We aimed to determine whether diaphragm muscle weakness is 1) early-onset post-MI (i.e., within the early left ventricular remodeling phase of 72 h); and 2) associated with elevated protein oxidation. Ligation of the left coronary artery to induce MI (n = 10) or sham operation (n = 10) was performed on C57BL6 mice. In vitro contractile function of diaphragm muscle fiber bundles was assessed 72 h later. Diaphragm mRNA and protein expression, enzyme activity, and individual carbonylated proteins (by two-dimensional differential in-gel electrophoresis and mass spectrometry) were subsequently assessed. Infarct size averaged 57 ± 1%. Maximal diaphragm function was reduced (P < 0.01) by 20% post-MI, with the force-frequency relationship depressed (P < 0.01) between 80 and 300 Hz. The mRNA expression of inflammation, atrophy, and regulatory Ca(2+) proteins remained unchanged post-MI, as did the protein expression of key contractile proteins. However, enzyme activity of the oxidative sources NADPH oxidase and xanthine oxidase was increased (P < 0.01) by 45 and 33%, respectively. Compared with sham, a 57 and 45% increase (P < 0.05) was observed in the carbonylation of sarcomeric actin and creatine kinase post-MI, respectively. In conclusion, diaphragm muscle weakness was rapidly induced in mice during the early left ventricular remodeling phase of 72 h post-MI, which was associated with increased oxidation of contractile and energetic proteins. Collectively, these findings suggest diaphragm muscle weakness may be early onset in heart failure, which is likely mediated in part by posttranslational oxidative modifications at the myofibrillar level.
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