ArticleMolecular & cellular proteomics : MCP2014
Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.
Article in Molecular & cellular proteomics : MCP, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Dual AAV gene therapy using laminin-linking proteins ameliorates muscle and nerve defects in LAMA2-related muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- Spatial proteomics reveals recombinant human laminin-111 restores adhesion signaling to laminin-α2-deficient muscle.JCI insight · 2025Article
- A novel mouse model foreLife · 2025Article
- Targeting Galectin-3 to modulate inflammation in LAMA2-deficient congenital muscular dystrophy.bioRxiv : the preprint server for biology · 2025Article
- Laminin-α2 chain deficiency in skeletal muscle causes dysregulation of multiple cellular mechanisms.Life science alliance · 2024Article
- Thrombospondin-4 deletion does not exacerbate muscular dystrophy in β-sarcoglycan-deficient and laminin α2 chain-deficient mice.Scientific reports · 2024Article
- Vemurafenib improves muscle histopathology in a mouse model of LAMA2-related congenital muscular dystrophy.Disease models & mechanisms · 2023Article
- Merosin deficient congenital muscular dystrophy type 1A: An international workshop on the road to therapy 15-17 November 2019, Maastricht, the Netherlands.Neuromuscular disorders : NMD · 2021Article
- Extracellular matrix: an important regulator of cell functions and skeletal muscle development.Cell & bioscience · 2021Review
- Linking Oxidative Stress and DNA Damage to Changes in the Expression of Extracellular Matrix Components.Frontiers in genetics · 2021Review
- Purification of sarcoplasmic reticulum vesicles from horse gluteal muscle.Analytical biochemistry · 2020Article
- Antioxidants Reduce Muscular Dystrophy in theAntioxidants (Basel, Switzerland) · 2020Article
- LAMA2-Related Dystrophies: Clinical Phenotypes, Disease Biomarkers, and Clinical Trial Readiness.Frontiers in molecular neuroscience · 2020Review
- A Family of Laminin α2 Chain-Deficient Mouse Mutants: Advancing the Research on LAMA2-CMD.Frontiers in molecular neuroscience · 2020Review
- Impaired Regeneration in Dystrophic Muscle-New Target for Therapy.Frontiers in molecular neuroscience · 2020Article
- Early skeletal muscle pathology and disease progress in the dyScientific reports · 2019Article
- Identification of Candidate Protein Markers in Skeletal Muscle of Laminin-211-Deficient CMD Type 1A-Patients.Frontiers in neurology · 2019Article
- Effects of metformin on congenital muscular dystrophy type 1A disease progression in mice: a gender impact study.Scientific reports · 2018Article
- Exploratory Profiling of Urine MicroRNAs in thePLoS currents · 2018Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital muscular dystrophy with laminin α2 chain deficiency (MDC1A) is one of the most severe forms of muscular disease and is characterized by severe muscle weakness and delayed motor milestones. The genetic basis of MDC1A is well known, yet the secondary mechanisms ultimately leading to muscle degeneration and subsequent connective tissue infiltration are not fully understood. In order to obtain new insights into the molecular mechanisms underlying MDC1A, we performed a comparative proteomic analysis of affected muscles (diaphragm and gastrocnemius) from laminin α2 chain-deficient dy(3K)/dy(3K) mice, using multidimensional protein identification technology combined with tandem mass tags. Out of the approximately 700 identified proteins, 113 and 101 proteins, respectively, were differentially expressed in the diseased gastrocnemius and diaphragm muscles compared with normal muscles. A large portion of these proteins are involved in different metabolic processes, bind calcium, or are expressed in the extracellular matrix. Our findings suggest that metabolic alterations and calcium dysregulation could be novel mechanisms that underlie MDC1A and might be targets that should be explored for therapy. Also, detailed knowledge of the composition of fibrotic tissue, rich in extracellular matrix proteins, in laminin α2 chain-deficient muscle might help in the design of future anti-fibrotic treatments. All MS data have been deposited in the ProteomeXchange with identifier PXD000978 (http://proteomecentral.proteomexchange.org/dataset/PXD000978).
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