ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010
Laminin-111: a potential therapeutic agent for Duchenne muscular dystrophy.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 59 citations in OpenAlex.
- Palmitate promotes liver metastases by decreasing neutrophil antitumour behaviour.Nature metabolism · 2026Article
- Article
- Spatial proteomics reveals recombinant human laminin-111 restores adhesion signaling to laminin-α2-deficient muscle.JCI insight · 2025Article
- A new insight on alleviating the inhibitory effect of aflatoxin B1 on muscle development in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Extracellular matrix: the critical contributor to skeletal muscle regeneration-a comprehensive review.Inflammation and regeneration · 2023Review
- Lipin1 plays complementary roles in myofibre stability and regeneration in dystrophic muscles.The Journal of physiology · 2023Article
- Exogenous laminin exhibits a unique vascular pattern in the brain via binding to dystroglycan and integrins.Fluids and barriers of the CNS · 2022Article
- Biomimetic sponges improve muscle structure and function following volumetric muscle loss.Journal of biomedical materials research. Part A · 2021Article
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Extracellular matrix: an important regulator of cell functions and skeletal muscle development.Cell & bioscience · 2021Review
- Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.Frontiers in molecular neuroscience · 2020Article
- Zebrafish Models ofFrontiers in molecular neuroscience · 2020Article
- Laminin-111 protein therapy enhances muscle regeneration and repair in the GRMD dog model of Duchenne muscular dystrophy.Human molecular genetics · 2019Article
- The Effect of Laminin-111 Hydrogels on Muscle Regeneration in a Murine Model of Injury.Tissue engineering. Part A · 2019Article
- Regulation of Myogenic Activity by Substrate and Electrical StimulationBioResearch open access · 2019Article
- Cellular rescue in a zebrafish model of congenital muscular dystrophy type 1A.NPJ Regenerative medicine · 2019Article
- Treating pediatric neuromuscular disorders: The future is now.American journal of medical genetics. Part A · 2018Review
- Increased Expression of Laminin Subunit Alpha 1 Chain by dCas9-VP160.Molecular therapy. Nucleic acids · 2017Article
- Laminin: loss-of-function studies.Cellular and molecular life sciences : CMLS · 2017Review
- Laminin differentially regulates the stemness of type I and type II pericytes.Stem cell research & therapy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) still needs effective treatments, and myoblast transplantation (MT) is considered as an approach to repair damaged skeletal muscles. DMD is due to the complete loss of dystrophin from muscles. The lack of link between the contracting apparatus and the extracellular matrix leads to frequent damage to the sarcolemma triggering muscle fiber necrosis. Laminins are major proteins in the extracellular matrix. Laminin-111 is normally present in skeletal and cardiac muscles in mice and humans but only during embryonic development. In this study, we showed that intramuscular injection of laminin-111 increased muscle strength and resistance in mdx mice. We also used laminin-111 as a coadjuvant in MT, and we showed this protein decreased considerably the repetitive cycles of degeneration, inflammatory reaction, and regeneration. Moreover, MT is significantly improved. To explain the improvement, we confirmed with the same myoblast cell batch that laminin-111 improves proliferation and drastically increases migration in vitro. These results are extremely important because DMD could be treated only by the injection of a recombinant protein, a simple and safe therapy to prevent loss of muscle function. Moreover, the improvement in MT would be significant to treat the muscles of DMD patients who are already weak.
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.