ArticleAmerican journal of physiology. Cell physiology2015
SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- Antioxidants to prevent respiratory decline in people with Duchenne muscular dystrophy and progressive respiratory decline.The Cochrane database of systematic reviews · 2021Pooled it
- Antioxidants to prevent respiratory decline in people with Duchenne muscular dystrophy and progressive respiratory decline.The Cochrane database of systematic reviews · 2021Pooled it
- DWORF Gene Therapy Improves Cardiac Calcium Handling and Mitochondrial Function.Circulation research · 2025Article
- DWORF expression is reduced in a large animal model of Duchenne muscular dystrophy.Disease models & mechanisms · 2025Article
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- LED therapy modulates M1/M2 macrophage phenotypes and mitigates dystrophic features in treadmill-trained mdx mice.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024Article
- SERCA1 Overexpression in Skeletal Muscle Attenuates Muscle Atrophy and Improves Motor Function in a Mouse Model of ALS.Journal of neuromuscular diseases · 2024Article
- Profiling of Chromatin Accessibility in Pigs across Multiple Tissues and Developmental Stages.International journal of molecular sciences · 2023Article
- Curcumin Administration Improves Force ofAntioxidants (Basel, Switzerland) · 2023Article
- 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
- Multi-omics analysis of sarcospan overexpression in mdx skeletal muscle reveals compensatory remodeling of cytoskeleton-matrix interactions that promote mechanotransduction pathways.Skeletal muscle · 2023Article
- Ketogenic diet containing medium-chain triglyceride ameliorates transcriptome disruption in skeletal muscles of rat models of duchenne muscular dystrophy.Biochemistry and biophysics reports · 2022Article
- Mineralocorticoid receptor antagonists and glucocorticoids differentially affect skeletal muscle inflammation and pathology in muscular dystrophy.JCI insight · 2022Article
- Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Mechanisms of weakness in Mdx muscle following in vivo eccentric contractions.Journal of muscle research and cell motility · 2022Article
- Loss of α-actinin-3 confers protection from eccentric contraction damage in fast-twitch EDL muscles from aged mdx dystrophic mice by reducing pathological fibre branching.Human molecular genetics · 2022Article
- Targeting the Ubiquitin-Proteasome System in Limb-Girdle Muscular Dystrophy With CAPN3 Mutations.Frontiers in cell and developmental biology · 2022Article
- The SarcoEndoplasmic Reticulum Calcium ATPase (SERCA) pump: a potential target for intervention in aging and skeletal muscle pathologies.Skeletal muscle · 2021Review
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle wasting secondary to repeated muscle damage and inadequate repair. Elevations in intracellular free Ca²⁺ have been implicated in disease progression, and sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase 1 (SERCA1) overexpression has been shown to ameliorate the dystrophic phenotype in mdx mice. The purpose of this study was to assess the effects of SERCA1 overexpression in the more severe mdx/Utr(-/-) mouse model of DMD. Mice overexpressing SERCA1 were crossed with mdx/Utr ± mice to generate mdx/Utr(-/-)/+SERCA1 mice and compared with wild-type (WT), WT/+SERCA1, mdx/+SERCA1, and genotype controls. Mice were assessed at ∼12 wk of age for changes in Ca²⁺ handling, muscle mass, quadriceps torque, markers of muscle damage, and response to repeated eccentric contractions. SERCA1-overexpressing mice had a two- to threefold increase in maximal sarcoplasmic reticulum Ca²⁺-ATPase activity compared with WT which was associated with normalization in body mass for both mdx/+SERCA1 and mdx/Utr(-/-)/+SERCA1. Torque deficit in the quadriceps after eccentric injury was 2.7-fold greater in mdx/Utr(-/-) vs. WT mice, but only 1.5-fold greater in mdx/Utr(-/-)/+SERCA1 vs. WT mice, an attenuation of 44%. Markers of muscle damage (% centrally nucleated fibers, necrotic area, and serum creatine kinase levels) were higher in both mdx and mdx/Utr(-/-) vs. WT, and all were attenuated by overexpression of SERCA1. These data indicate that SERCA1 overexpression ameliorates functional impairments and cellular markers of damage in a more severe mouse model of DMD. These findings support targeting intracellular Ca²⁺ control as a therapeutic approach for DMD.
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.