ArticlePloS one2014
Poloxamer [corrected] 188 has a deleterious effect on dystrophic skeletal muscle function.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Current and Emerging Therapeutic Strategies for the Treatment of Duchenne Muscular Dystrophy.Genes · 2026Review
- Spatiotemporal analysis of dystrophin expression during muscle repair.Skeletal muscle · 2025Article
- Muscular Dystrophies.Advances in experimental medicine and biology · 2025Review
- Prkd1 regulates the formation and repair of plasma membrane disruptions (PMD) in osteocytes.Bone · 2024Article
- Review
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- The skeletal muscle phenotype of the DE50-MD dog model of Duchenne muscular dystrophy.Wellcome open research · 2022Article
- Regulation of excitation-contraction coupling at the Drosophila neuromuscular junction.The Journal of physiology · 2022Article
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.International journal of molecular sciences · 2021Review
- Review
- Exosome-mediated improvement in membrane integrity and muscle function in dystrophic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Simvastatin Treatment Does Not Ameliorate Muscle Pathophysiology in a Mouse Model for Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2021Article
- Ischemia reperfusion injury provokes adverse left ventricular remodeling in dysferlin-deficient hearts through a pathway that involves TIRAP dependent signaling.Scientific reports · 2020Article
- Therapeutic developments for Duchenne muscular dystrophy.Nature reviews. Neurology · 2019Review
- Muscle membrane integrity in Duchenne muscular dystrophy: recent advances in copolymer-based muscle membrane stabilizers.Skeletal muscle · 2018Review
- Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy.Expert opinion on orphan drugs · 2016Article
- Plasma Membrane Repair in Health and Disease.Current topics in membranes · 2016Review
- How much dystrophin is enough: the physiological consequences of different levels of dystrophin in the mdx mouse.Human molecular genetics · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked, fatal muscle wasting disease for which there is currently no cure and limited palliative treatments. Poloxomer 188 (P188) is a tri-block copolymer that has been proposed as a potential treatment for cardiomyopathy in DMD patients. Despite the reported beneficial effects of P188 on dystrophic cardiac muscle function, the effects of P188 on dystrophic skeletal muscle function are relatively unknown. Mdx mice were injected intraperitoneally with 460 mg/kg or 30 mg/kg P188 dissolved in saline, or saline alone (control). The effect of single-dose and 2-week daily treatment was assessed using a muscle function test on the Tibialis Anterior (TA) muscle in situ in anaesthetised mice. The test comprises a warm up, measurement of the force-frequency relationship and a series of eccentric contractions with a 10% stretch that have previously been shown to cause a drop in maximum force in mdx mice. After 2 weeks of P188 treatment at either 30 or 460 mg/kg/day the drop in maximum force produced following eccentric contractions was significantly greater than that seen in saline treated control mice (P = 0.0001). Two week P188 treatment at either dose did not significantly change the force-frequency relationship or maximum isometric specific force produced by the TA muscle. In conclusion P188 treatment increases susceptibility to contraction-induced injury following eccentric contractions in dystrophic skeletal muscle and hence its suitability as a potential therapeutic for DMD should be reconsidered.
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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.