ArticleNeurochemical research2013
Oxidative stress, NF-κB and the ubiquitin proteasomal pathway in the pathology of calpainopathy.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Inflammation-Linked Muscle Atrophy in Limb Girdle Muscular Dystrophy R1 (LGMDR1): Insights into Disease Mechanisms.Current issues in molecular biology · 2026Article
- Recent insights into limb-girdle muscular dystrophy: Impacts, therapy, and challenges.Histology and histopathology · 2025Review
- Dose-response effect of L-citrulline on skeletal muscle damage after acute eccentric exercise: anPeerJ · 2023Article
- Antrodia camphorata polysaccharide improves inflammatory response in liver injury via the ROS/TLR4/NF-κB signal.Journal of cellular and molecular medicine · 2022Article
- Targeting the Ubiquitin-Proteasome System in Limb-Girdle Muscular Dystrophy With CAPN3 Mutations.Frontiers in cell and developmental biology · 2022Article
- Systemic delivery of AAVrh74.tMCK.hCAPN3 rescues the phenotype in a mouse model for LGMD2A/R1.Molecular therapy. Methods & clinical development · 2021Article
- Redox Homeostasis in Muscular Dystrophies.Cells · 2021Review
- Calcium Mechanisms in Limb-Girdle Muscular Dystrophy withInternational journal of molecular sciences · 2019Review
- Calpain 3 deficiency affects SERCA expression and function in the skeletal muscle.Expert reviews in molecular medicine · 2016Article
- Eosinophilic esophagitis-linked calpain 14 is an IL-13-induced protease that mediates esophageal epithelial barrier impairment.JCI insight · 2016Article
- The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes.Journal of muscle research and cell motility · 2015Review
- Altered ubiquitin causes perturbed calcium homeostasis, hyperactivation of calpain, dysregulated differentiation, and cataract.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Skeletal muscle tissue engineering: methods to form skeletal myotubes and their applications.Tissue engineering. Part B, Reviews · 2014Review
- Redox state and mitochondrial respiratory chain function in skeletal muscle of LGMD2A patients.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuromuscular disorder, calpainopathy (LGMD 2A), is a major muscular dystrophy classified under limb girdle muscular dystrophies. Genetic mutations of the enzyme calpain 3 cause LGMD 2A. Calpainopathy is phenotypically observed as progressive muscle wasting and weakness. Pathomechanisms of muscle wasting of calpainopathy remain poorly understood. Oxidative stress, NF-κB and the ubiquitin proteasomal pathway underlie the pathology of several muscle wasting conditions but their role in calpainopathic dystrophy is not known. Oxidative and nitrosative stress, the source of reactive oxygen species, NF-κB signaling and protein ubiquitinylation were studied in 15 calpainopathic and 8 healthy control human muscle biopsies. Oxidative stress and NF-κB/IKK β signaling were increased in calpainopathic muscle and may contribute to increased protein ubiquitinylation and muscle protein loss. Preventing oxidative stress or inhibition of NF-κB signaling could be considered for treatment of LGMD 2A.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.