ArticleMethods in molecular biology (Clifton, N.J.)2011
Monitoring murine skeletal muscle function for muscle gene therapy.
Article in Methods in molecular biology (Clifton, N.J.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 62 citations in OpenAlex.
- Exacerbated Skeletal Muscle Phenotype in Mice with 'Homotypic' Expression of the Tubular Aggregate Myopathy ORAI1 G100S Mutation.Biomedicines · 2026Article
- An Orai1 gain-of-function tubular aggregate myopathy mouse model phenocopies key features of the human disease.The EMBO journal · 2024Article
- Age-associated functional healing of musculoskeletal trauma through regenerative engineering and rehabilitation.Biomaterials science · 2024Article
- Constitutive, Muscle-SpecificBiomedicines · 2024Article
- SERCA2a overexpression improves muscle function in a canine Duchenne muscular dystrophy model.Molecular therapy. Methods & clinical development · 2024Article
- Verapamil mitigates chloride and calcium bi-channelopathy in a myotonic dystrophy mouse model.The Journal of clinical investigation · 2024Article
- Persistence of exon 2 skipping and dystrophin expression at 18 months after U7snRNA-mediated therapy in the Dup2 mouse model.Molecular therapy. Methods & clinical development · 2023Article
- Expression and function of four AAV-based constructs for dystrophin restoration in the mdx mouse model of Duchenne muscular dystrophy.Biology open · 2023Article
- The Implication of Hinge 1 and Hinge 4 in Micro-Dystrophin Gene Therapy for Duchenne Muscular Dystrophy.Human gene therapy · 2023Article
- Lifelong Outcomes of Systemic Adeno-Associated Virus Micro-Dystrophin Gene Therapy in a Murine Duchenne Muscular Dystrophy Model.Human gene therapy · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- BMP-7 Attenuates Sarcopenia and Adverse Muscle Remodeling in Diabetic Mice via Alleviation of Lipids, Inflammation, HMGB1, and Pyroptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Physiological Assessment of Muscle, Heart, and Whole Body Function in the Canine Model of Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Semirational bioengineering of AAV vectors with increased potency and specificity for systemic gene therapy of muscle disorders.Science advances · 2022Article
- Systemic delivery of an AAV9 exon-skipping vector significantly improves or prevents features of Duchenne muscular dystrophy in the Dup2 mouse.Molecular therapy. Methods & clinical development · 2022Article
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- Rational engineering of a functional CpG-free ITR for AAV gene therapy.Gene therapy · 2022Article
- The gRNA Vector Level Determines the Outcome of Systemic AAV CRISPR Therapy for Duchenne Muscular Dystrophy.Human gene therapy · 2022Article
- Extensor carpi ulnaris muscle shows unexpected slow-to-fast fiber-type switch in Duchenne muscular dystrophy dogs.Disease models & mechanisms · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The primary function of skeletal muscle is to generate force. Muscle force production is compromised in various forms of acquired and/or inherited muscle diseases. An important goal of muscle gene therapy is to recover muscle strength. Genetically engineered mice and spontaneous mouse mutants are readily available for preclinical muscle gene therapy studies. In this chapter, we outlined the methods commonly used for measuring murine skeletal muscle function. These include ex vivo and in situ analysis of the contractile profile of a single intact limb muscle (the extensor digitorium longus for ex vivo assay and the tibialis anterior muscle for in situ assay), grip force analysis, and downhill treadmill exercise. Force measurement in a single muscle is extremely useful for pilot testing of new gene therapy protocols by local gene transfer. Grip force and treadmill assessments offer body-wide evaluation following systemic muscle gene therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.