ReviewMolecular and cellular biochemistry1999
Mechanisms of resistance to pathogenesis in muscular dystrophies.
Review in Molecular and cellular biochemistry, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 27 citations in OpenAlex.
- Muscle metabolic remodelling patterns in Duchenne muscular dystrophy revealed by ultra-high-resolution mass spectrometry imaging.Scientific reports · 2021Article
- Microutrophin expression in dystrophic mice displays myofiber type differences in therapeutic effects.PLoS genetics · 2020Article
- Protein 4.1R Influences Myogenin Protein Stability and Skeletal Muscle Differentiation.The Journal of biological chemistry · 2016Article
- Discovery of serum protein biomarkers in the mdx mouse model and cross-species comparison to Duchenne muscular dystrophy patients.Human molecular genetics · 2014Article
- Dystrophin and utrophin "double knockout" dystrophic mice exhibit a spectrum of degenerative musculoskeletal abnormalities.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2013Article
- Functional muscle analysis of the Tcap knockout mouse.Human molecular genetics · 2010Article
- Correlation of circulating CD133+ progenitor subclasses with a mild phenotype in Duchenne muscular dystrophy patients.PloS one · 2008Article
- Gender dimorphism influences extracellular matrix expression and regeneration of muscular tissue in mdx dystrophic mice.Histochemistry and cell biology · 2004Article
- Resolution of skeletal muscle inflammation in mdx dystrophic mouse is accompanied by increased immunoglobulin and interferon-gamma production.International journal of experimental pathology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A mechanistic definition of the dystrophic process is proposed, and the effects of growth factors vs. down-regulation of growth are critically analyzed. A conceptual scheme is presented to illustrate the steps leading to pathology, and various compensatory systems which ameliorate the pathology are examined, particularly in regards to the mdv mouse which is resistant to the deficiency of dystrophin, the main protein product of the Duchenne and Becker muscular dystrophy (DMD/BMD) gene. These compensatory systems are analyzed in terms of the differential resistance of fiber types to pathogenesis. The generation of a stable population of maturationally arrested centronucleated fibers which express the mature adult myosin isoforms is proposed to be the main strategy of mdx muscle to minimize apoptosis. Physiological properties of these fibers, such as utrophin expression, and high mitochondrial and endoplasmic reticulum content, together with probable increased glycerophosphorylcholine concentrations and facile access to the vascular system, are hypothesized to be instrumental in their resistance to pathogenesis. It is proposed that the major element that determines the susceptibility of most human muscles to the dystrophic process is their inability to arrest the maturation of regenerated fibers at the centronucleated stage with a concomitant expression of the adult myosins.
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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.