ArticleCell death and differentiation2012
Necdin enhances muscle reconstitution of dystrophic muscle by vessel-associated progenitors, by promoting cell survival and myogenic differentiation.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis.Molecular therapy. Methods & clinical development · 2019Review
- Pericytes in Muscular Dystrophies.Advances in experimental medicine and biology · 2019Article
- Concise review: mesoangioblast and mesenchymal stem cell therapy for muscular dystrophy: progress, challenges, and future directions.Stem cells translational medicine · 2015Review
- The alpha subunit of Go modulates cell proliferation and differentiation through interactions with Necdin.Cell communication and signaling : CCS · 2014Article
- Necdin, a p53 target gene, in stem cells.Oncotarget · 2013Article
- Requirement of inducible nitric oxide synthase for skeletal muscle regeneration after acute damage.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Necdin enhances myoblasts survival by facilitating the degradation of the mediator of apoptosis CCAR1/CARP1.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Improving stem cell therapy is a major goal for the treatment of muscle diseases, where physiological muscle regeneration is progressively exhausted. Vessel-associated stem cells, such as mesoangioblasts (MABs), appear to be the most promising cell type for the cell therapy for muscular dystrophies and have been shown to significantly contribute to restoration of muscle structure and function in different muscular dystrophy models. Here, we report that melanoma antigen-encoding gene (MAGE) protein necdin enhances muscle differentiation and regeneration by MABs. When necdin is constitutively overexpressed, it accelerates their differentiation and fusion in vitro and it increases their efficacy in reconstituting regenerating myofibres in the α-sarcoglycan dystrophic mouse. Moreover, necdin enhances survival when MABs are exposed to cytotoxic stimuli that mimic the inflammatory dystrophic environment. Taken together, these data demonstrate that overexpression of necdin may be a crucial tool to boost therapeutic applications of MABs in dystrophic muscle.
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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.