ArticleFrontiers in molecular neuroscience2020
Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 70 citations in OpenAlex.
- Laminin α5 and integrins α3 and α6 coordinately regulate collective cell migration in vivo.Development (Cambridge, England) · 2026Article
- Clinical and functional outcome measures in LAMA2-related muscular dystrophy and SELENON-related myopathy; a 1.5-year natural history study.Journal of neuromuscular diseases · 2026Article
- Recovery From Heart Failure: Microvascular Mechanisms.Circulation · 2026Article
- 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
- A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies.bioRxiv : the preprint server for biology · 2025Article
- Immunocytochemistry response of a hybrid (chitosan-RSC advances · 2025Article
- Laminin-derived peptide drives the cardiomyogenic potential and cardiac cells functionality.Frontiers in bioengineering and biotechnology · 2025Article
- Sil1-deficient fibroblasts generate an aberrant extracellular matrix leading to tendon disorganisation in Marinesco-Sjögren syndrome.Journal of translational medicine · 2024Article
- Molecular mechanisms and therapeutic strategies for neuromuscular diseases.Cellular and molecular life sciences : CMLS · 2024Review
- The congenital muscular dystrophies.Annals of the Child Neurology Society · 2024Review
- Cardiac Involvement in LAMA2-Related Muscular Dystrophy and SELENON-Related Congenital Myopathy: A Case Series.Journal of neuromuscular diseases · 2024Article
- Article
- Odd skipped-related 1 controls the pro-regenerative response of fibro-adipogenic progenitors.NPJ Regenerative medicine · 2023Article
- The alpha7 integrin subunit in astrocytes promotes endothelial blood-brain barrier integrity.Development (Cambridge, England) · 2023Article
- The emergence of the stem cell niche.Trends in cell biology · 2023Review
- Novel compound heterozygous mutations of LAMA2-limb-girdle muscular dystrophy: A case report and literature review.Frontiers in neurology · 2023Article
- Lama2 And Samsn1 Mediate the Effects of Brn4 on Hippocampal Neural Stem Cell Proliferation and Differentiation.Stem cells international · 2023Article
- Merosin-deficient congenital muscular dystrophy type 1a: detection ofFrontiers in genetics · 2023Article
- Methylation- and homologous recombination deficiency-related mutant genes predict the prognosis of lung adenocarcinoma.Journal of clinical laboratory analysis · 2022Article
- DNA Repair and Replication-Related Gene Signature Based on Tumor Mutation Burden Reveals Prognostic and Immunotherapy Response in Gastric Cancer.Journal of oncology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laminin-α2-related congenital muscular dystrophy (LAMA2-CMD) is a devastating neuromuscular disease caused by mutations in the LAMA2 gene. These mutations result in the complete absence or truncated expression of the laminin-α2 chain. The α2-chain is a major component of the laminin-211 and laminin-221 isoforms, the predominant laminin isoforms in healthy adult skeletal muscle. Mutations in this chain result in progressive skeletal muscle degeneration as early as neonatally. Laminin-211/221 is a ligand for muscle cell receptors integrin-α7β1 and α-dystroglycan. LAMA2 mutations are correlated with integrin-α7β1 disruption in skeletal muscle. In this review, we will summarize laminin-211/221 interactions with integrin-α7β1 in LAMA2-CMD muscle. Additionally, we will summarize recent developments using upregulation of laminin-111 in the sarcolemma of laminin-α2-deficient muscle. We will discuss potential mechanisms of action by which laminin-111 is able to prevent myopathy. These published studies demonstrate that laminin-111 is a disease modifier of LAMA2-CMD through different methods of delivery. Together, these studies show the potential for laminin-111 therapy as a novel paradigm for the treatment of LAMA2-CMD.
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