ReviewThe FEBS journal2013
The potential of sarcospan in adhesion complex replacement therapeutics for the treatment of muscular dystrophy.
Review in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2025Review
- The Development of Robust Antibodies to Sarcospan, a Dystrophin- and Integrin-Associated Protein, for Basic and Translational Research.International journal of molecular sciences · 2024Article
- Myoscaffolds reveal laminin scarring is detrimental for stem cell function while sarcospan induces compensatory fibrosis.NPJ Regenerative medicine · 2023Article
- Sarcospan increases laminin-binding capacity of α-dystroglycan to ameliorate DMD independent of Galgt2.Human molecular genetics · 2022Article
- Development of a high-throughput screen to identify small molecule enhancers of sarcospan for the treatment of Duchenne muscular dystrophy.Skeletal muscle · 2019Article
- Lectin-binding characterizes the healthy human skeletal muscle glycophenotype and identifies disease-specific changes in dystrophic muscle.Glycobiology · 2017Article
- High levels of sarcospan are well tolerated and act as a sarcolemmal stabilizer to address skeletal muscle and pulmonary dysfunction in DMD.Human molecular genetics · 2016Article
- CD82 Is a Marker for Prospective Isolation of Human Muscle Satellite Cells and Is Linked to Muscular Dystrophies.Cell stem cell · 2016Article
- Current and emerging treatment strategies for Duchenne muscular dystrophy.Neuropsychiatric disease and treatment · 2016Review
- Sarcospan Regulates Cardiac Isoproterenol Response and Prevents Duchenne Muscular Dystrophy-Associated Cardiomyopathy.Journal of the American Heart Association · 2015Article
- Mending a Broken Heart: The Role of Sarcospan in Duchenne Muscular Dystrophy-Associated Cardiomyopathy.Journal of the American Heart Association · 2015Article
- Sarcospan integration into laminin-binding adhesion complexes that ameliorate muscular dystrophy requires utrophin and α7 integrin.Human molecular genetics · 2015Article
- Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy.Disease models & mechanisms · 2015Review
- Muscle structure influences utrophin expression in mdx mice.PLoS genetics · 2014Article
- Meeting Report: New Directions in the Biology and Disease of Skeletal Muscle 2014.Journal of neuromuscular diseases · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Three adhesion complexes span the sarcolemma and facilitate critical connections between the extracellular matrix and the actin cytoskeleton: the dystrophin- and utrophin-glycoprotein complexes and α7β1 integrin. Loss of individual protein components results in a loss of the entire protein complex and muscular dystrophy. Muscular dystrophy is a progressive, lethal wasting disease characterized by repetitive cycles of myofiber degeneration and regeneration. Protein-replacement therapy offers a promising approach for the treatment of muscular dystrophy. Recently, we demonstrated that sarcospan facilitates protein-protein interactions amongst the adhesion complexes and is an important potential therapeutic target. Here, we review current protein-replacement strategies, discuss the potential benefits of sarcospan expression, and identify important experiments that must be addressed for sarcospan to move to the clinic.
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What Socratic 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 Socratic graph.