ArticleJournal of muscle research and cell motility2003
Recovery of contractile and metabolic phenotypes in regenerating slow muscle after notexin-induced or crush injury.
Article in Journal of muscle research and cell motility, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 47 citations in OpenAlex.
- Regenerating Myofibers after an Acute Muscle Injury: What Do We Really Know about Them?International journal of molecular sciences · 2023Review
- Cardiotoxin-induced skeletal muscle injury elicits profound changes in anabolic and stress signaling, and muscle fiber type composition.Journal of muscle research and cell motility · 2020Article
- Ibuprofen does not impair skeletal muscle regeneration upon cardiotoxin-induced injury.Physiological research · 2020Article
- EDMD-Causing Emerin Mutant Myogenic Progenitors Exhibit Impaired Differentiation Using Similar Mechanisms.Cells · 2020Article
- Mitochondrial protein S-nitrosation protects against ischemia reperfusion-induced denervation at neuromuscular junction in skeletal muscle.Free radical biology & medicine · 2018Article
- Plasticity of the Muscle Stem Cell Microenvironment.Advances in experimental medicine and biology · 2017Review
- Extracellular matrix regulation in the muscle satellite cell niche.Connective tissue research · 2015Review
- Effect of hypoxia exposure on the recovery of skeletal muscle phenotype during regeneration.Molecular and cellular biochemistry · 2014Article
- Ambient hypoxia enhances the loss of muscle mass after extensive injury.Pflugers Archiv : European journal of physiology · 2014Article
- Article
- Mitochondria as a potential regulator of myogenesis.TheScientificWorldJournal · 2013Review
- Muscle regeneration occurs to coincide with mitochondrial biogenesis.Molecular and cellular biochemistry · 2011Article
- Time course of skeletal muscle regeneration after severe trauma.Acta orthopaedica · 2011Article
- mTOR regulates skeletal muscle regeneration in vivo through kinase-dependent and kinase-independent mechanisms.American journal of physiology. Cell physiology · 2009Article
- Regeneration of reinnervated rat soleus muscle is accompanied by fiber transition toward a faster phenotype.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2008Article
- Changes in contractile activation characteristics of rat fast and slow skeletal muscle fibres during regeneration.The Journal of physiology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The recovery of metabolic pathways after muscle damage has been poorly studied. We investigated the myosin heavy chain (MHC) isoform transitions and the recovery of citrate synthase (CS) activity, isoform distribution of lactate dehydrogenase (LDH) and creatine kinase (CK) in slow muscles after two types of injury. Muscle degeneration was induced in left soleus muscles of male Wistar rats by either notexin injection or crushing and the regenerative process was examined from 2 to 56 days after injury. Myosin transition occurred earlier after notexin than after crush injury. Fast-type IIx and more particularly type IIa MHC isoform disappeared by day 28 after notexin inoculation, while they were still detected long after in crushed muscles. A full recovery of both the CS activity and the specific activity of the H-LDH subunit was observed from day 42 in notexin-treated muscles, while values measured in crushed muscles remained significantly lower than in non-injured muscles (P < 0.05). The activity of the mitochondrial isoform of CK (mi-CK) was markedly affected by the type of injury (P < 0.001), and failed to reach normal levels after crush injury (P < 0.05). The results of this study show that the relatively rapid MHC transitions during regeneration contrasts with the slow recovery in the oxidative capacity. The recovery of the oxidative capacity remained incomplete after crush injury, a model of injury known to lead to disruption of the basal lamina and severe interruption of the vascular and nerve supply.
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