ArticleSkeletal muscle2017
Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.
Article in Skeletal muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dyslipidemia in Muscular Dystrophy: A Systematic Review and Meta-Analysis.Journal of neuromuscular diseases · 2023Pooled it
- A high-fat, high-sucrose diet exacerbates muscle and metabolic pathology and undermines glucocorticoid efficacy in dystrophin-deficient mice.The Journal of physiology · 2026Article
- DAB2 in LGMD R2: a molecular link between disease progression and lipid dysregulation.JCI insight · 2026Article
- The miR-30c-5p/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2026Article
- Large-scale serum protein biomarkers discovery associated with function and clinical milestones in Duchenne muscular dystrophy.Nature communications · 2025Observational
- Intramuscular adipose tissue: from progenitor to pathology.American journal of physiology. Cell physiology · 2025Review
- Effects of HMG CoA reductase (HMGCR) deficiency on skeletal muscle development.The FEBS journal · 2025Article
- Intramuscular adipose tissue restricts functional muscle recovery.Cell reports · 2025Article
- Causal effect of severe and non-severe malaria on dyslipidemia in African Ancestry individuals: A Mendelian randomization study.Annals of human genetics · 2025Article
- miRNA dysregulation in Duchenne muscular dystrophy comorbidities.World journal of experimental medicine · 2025Article
- Association between triglycerides and remnant cholesterol levels and spine bone mineral density in Duchenne muscular dystrophy.Lipids in health and disease · 2025Article
- Pharmacology and macrophage modulation of HPGDS inhibitor PK007 demonstrate reduced disease severity in DMD-affected muscles of the mdx mouse model.Skeletal muscle · 2025Article
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice.Skeletal muscle · 2024Article
- Apolipoprotein E knockout, but not cholesteryl ester transfer protein (CETP)-associated high-density lipoprotein cholesterol (HDL-C) lowering, exacerbates muscle wasting in dysferlin-null mice.Lipids in health and disease · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- A fat- and sucrose-enriched diet causes metabolic alterations in mdx mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration.Nature communications · 2023Article
- Echo2Pheno: a deep-learning application to uncover echocardiographic phenotypes in conscious mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- Experimental evidence and clinical implications of Warburg effect in the skeletal muscle of Fabry disease.iScience · 2023Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is caused by loss of dystrophin expression and leads to severe ambulatory and cardiac function decline. However, the dystrophin-deficient mdx murine model of DMD only develops a very mild form of the disease. Our group and others have shown vascular abnormalities in animal models of MD, a likely consequence of the fact that blood vessels express the same dystrophin-associated glycoprotein complex (DGC) proteins as skeletal muscles.
methodsTo test the blood vessel contribution to muscle damage in DMD, mdx
resultsAlthough there was an increase in left ventricular heart volume in mdx-ApoE mice compared to that in mdx mice, parameters of heart function were not affected. Compared with wild-type and ApoE-null, only mdx-ApoE KO mice showed significant ambulatory dysfunction. Despite no significant difference in plasma CK, histological analyses revealed that elevated plasma lipids in chow- and Western diet-fed mdx-ApoE mice was associated with severe exacerbation of muscle pathology compared to mdx mice: significant increase in myofiber damage and fibrofatty replacement in the gastrocnemius and triceps brachii muscles, more reminiscent of human DMD pathology. Finally, although both ApoE and mdx-ApoE groups displayed increased plasma lipids, mdx-ApoE exhibited atherosclerotic plaque deposition equal to or less than that of ApoE mice.
conclusionsSince others have shown that lipid abnormalities correlate with DMD severity, our data suggest that plasma lipids could be primary contributors to human DMD severity and that the notoriously mild phenotype of mdx mice might be attributable in part to their endogenously low plasma lipid profiles. Hence, DMD patients may benefit from lipid-lowering and vascular-targeted therapies.
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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.