ArticleJournal of anatomy2003
Muscle fibre breakdown in venom-induced muscle degeneration.
Article in Journal of anatomy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 36 citations in OpenAlex.
- Alterations of the skeletal muscle contractile apparatus in necrosis induced by myotoxic snake venom phospholipases AJournal of muscle research and cell motility · 2024Review
- Review
- Effect of spaghetti meat abnormality on broiler chicken breast meat composition and technological quality.Poultry science · 2020Article
- Biotoxins in muscle regeneration research.Journal of muscle research and cell motility · 2019Review
- Attenuation of autophagy impacts on muscle fibre development, starvation induced stress and fibre regeneration following acute injury.Scientific reports · 2018Article
- Review
- Osteopontin deficiency delays inflammatory infiltration and the onset of muscle regeneration in a mouse model of muscle injury.Disease models & mechanisms · 2013Article
- Pulsed ultrasound therapy accelerates the recovery of skeletal muscle damage induced by Bothrops jararacussu venom.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012Article
- CD34 promotes satellite cell motility and entry into proliferation to facilitate efficient skeletal muscle regeneration.Stem cells (Dayton, Ohio) · 2011Article
- Muscle injury activates resident fibro/adipogenic progenitors that facilitate myogenesis.Nature cell biology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We studied the early stages of the degeneration of skeletal muscles using the venom of Notechis scutatus as the myotoxic agent. The venom was used at a dose equivalent to the LD50 in the mouse. There was no mortality amongst the rats. Electron microscopy was used to show the progressive hypercontraction of sarcomeres and the loss of alignment of myofibrils in individual muscle fibres. Between areas of hypercontraction sarcomeres were torn, shedding loosened myofilaments into the cytosol. Western blotting and Coomassie staining were used to compare the respective rates of loss of desmin, titin, actin, myosin and dystrophin. We showed that desmin and titin were the first proteins to be degraded with a time to 50% loss of approximately 1 h and 3 h, respectively. The loss of major contractile proteins, myosin and actin, was rather slower. The loss of dystrophin was also slower than the loss of desmin and titin. Early damage to the plasma membrane of the muscle fibre caused the cells to depolarize, probably promoting the hypercontraction of the sarcomeres, but actual loss of membrane was incomplete even at 24 h. We suggest that the early degradation of desmin and titin was responsible for the disaggregation of the sarcomeres; the liberated contractile proteins myosin and actin were shed into the cytosol, where they were degraded. Phagocytic cells that had invaded the degenerating muscle fibres were primarily involved in the clearance of damaged mitochondria.
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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.