ArticleBMC musculoskeletal disorders2011
Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology.
Article in BMC musculoskeletal disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Establishment of a novel rat model for deep tissue injury deterioration.International wound journal · 2015Article
- Myostatin Activates the Ubiquitin-Proteasome and Autophagy-Lysosome Systems Contributing to Muscle Wasting in Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2015Article
- SIRT1-dependent myoprotective effects of resveratrol on muscle injury induced by compression.Frontiers in physiology · 2015Article
- Leucine supplementation accelerates connective tissue repair of injured tibialis anterior muscle.Nutrients · 2014Article
- MicroRNAs as regulators of cutaneous wound healing.Journal of biosciences · 2014Review
- Oxidative stress and DNA damage signalling in skeletal muscle in pressure-induced deep tissue injury.Pflugers Archiv : European journal of physiology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular mechanism initiating deep pressure ulcer remains to be elucidated. The present study tested the hypothesis that the ubiquitin proteasome system is involved in the signalling mechanism in pressure-induced deep tissue injury.
methodsAdult Sprague Dawley rats were subjected to an experimental compression model to induce deep tissue injury. The tibialis region of the right hind limb was subjected to 100 mmHg of static pressure for six hours on each of two consecutive days. The compression pressure was continuously monitored by a three-axial force transducer within the compression indentor. The left hind limb served as the intra-animal control. Muscle tissues underneath the compressed region were collected and used for analyses.
resultsOur results demonstrated that the activity of 20S proteasome and the protein abundance of ubiquitin and MAFbx/atrogin-1 were elevated in conjunction with pathohistological changes in the compressed muscle, as compared to control muscle. The administration of the proteasome inhibitor MG132 was found to be effective in ameliorating the development of pathological histology in compressed muscle. Furthermore, 20S proteasome activity and protein content of ubiquitin and MAFbx/atrogin-1 showed no apparent increase in the MG132-treated muscle following compression.
conclusionOur data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury.
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