ArticleAmerican journal of respiratory cell and molecular biology2010
Calpain activation contributes to endotoxin-induced diaphragmatic dysfunction.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- Beyond muscle weakness: pathogenesis of sepsis-induced myopathy and its management.Open medicine (Warsaw, Poland) · 2026Review
- Role of GLP‑1 receptor agonists in sepsis and their therapeutic potential in sepsis‑induced muscle atrophy (Review).International journal of molecular medicine · 2025Review
- Predicting early diagnosis of intensive care unit-acquired weakness in septic patients using critical ultrasound and biological markers.BMC anesthesiology · 2025Observational
- Evaluation of the Anti-Amyloid and Anti-Inflammatory Properties of a Novel Vanadium(IV)-Curcumin Complex in Lipopolysaccharides-Stimulated Primary Rat Neuron-Microglia Mixed Cultures.International journal of molecular sciences · 2024Article
- Intensive care unit-acquired weakness: Recent insights.Journal of intensive medicine · 2024Review
- Autophagy ablation in skeletal muscles worsens sepsis-induced muscle wasting, impairs whole-body metabolism, and decreases survival.iScience · 2023Article
- Magnetic twitch assessment of diaphragm and quadriceps weakness in critically ill mechanically ventilated patients.Respiratory physiology & neurobiology · 2022Article
- Skeletal muscle-specific calpastatin overexpression mitigates muscle weakness in aging and extends life span.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Mitoquinone mesylate (MitoQ) prevents sepsis-induced diaphragm dysfunction.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Magnesium sulfate ameliorates sepsis-induced diaphragm dysfunction in rats via inhibiting HMGB1/TLR4/NF-κB pathway.Neuroreport · 2020Article
- MitoTEMPOL, a mitochondrial targeted antioxidant, prevents sepsis-induced diaphragm dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- SS31, a mitochondrially targeted antioxidant, prevents sepsis-induced reductions in diaphragm strength and endurance.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- α-Calcitonin gene-related peptide inhibits autophagy and calpain systems and maintains the stability of neuromuscular junction in denervated muscles.Molecular metabolism · 2019Article
- Hydrogen sulfide prevents diaphragm weakness in cecal ligation puncture-induced sepsis by preservation of mitochondrial function.American journal of translational research · 2017Article
- Dysfunction of respiratory muscles in critically ill patients on the intensive care unit.Journal of cachexia, sarcopenia and muscle · 2016Review
- Calcium-dependent phospholipase A2 modulates infection-induced diaphragm dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Neutral sphingomyelinase 2 is required for cytokine-induced skeletal muscle calpain activation.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- A conceptual framework: the early and late phases of skeletal muscle dysfunction in the acute respiratory distress syndrome.Critical care (London, England) · 2015Review
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- Dexmedetomidine May Produce Extra Protective Effects on Sepsis-induced Diaphragm Injury.Chinese medical journal · 2015Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calpain activation occurs in skeletal muscle in response to infection, but it is unknown if calpain inhibition improves muscle functional capacity. We hypothesized that infection induces diaphragm calpain activation, that calpain activation results in cleavage of important diaphragm cytoskeletal proteins, and that inhibition of calpain attenuates infection-induced diaphragm dysfunction. Mice (n = 4-6/group) were given: (1) saline (intraperitoneal); (2) endotoxin (12 mg/kg intraperitoneal); (3) calpain inhibitor peptide III (12 mg/kg intraperitoneal); and (4) endotoxin (12 mg/kg) plus calpain inhibitor peptide III (12 mg/kg). At 24 hours, diaphragms were removed and the following determined: (1) calpain activity by fluorogenic assay; (2) calpain I and II protein levels; (3) talin protein levels; and (4) the force-frequency relationship. Endotoxin significantly increased diaphragm calpain activity (P < 0.001), active calpain I protein (P < 0.001), active calpain II protein (P < 0.01), levels of a calpain-specific cleavage talin degradation product (P < 0.003), and reduced diaphragm force (P < 0.001). Calpain inhibitor III administration prevented endotoxin-induced increases in calpain activity, reduced talin degradation, and attenuated reductions in diaphragm force. Diaphragm-specific force at 150 Hz stimulation was significantly higher in control, endotoxin plus calpain inhibitor III, and calpain inhibitor III alone groups (23 +/- 1, 20 +/- 1 and 23 +/- 1 N/cm(2), respectively) than in the endotoxin alone group (15 +/- 1 N/cm(2)) (P < 0.01). This model of sepsis results in significant diaphragm calpain activation and calpain-dependent diaphragm cytoskeletal protein cleavage. Moreover, calpain inhibition attenuates endotoxin-induced diaphragm weakness, suggesting that such inhibitors may be a potential treatment to improve respiratory muscle function in infected patients.
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