Εμφάνιση απλής εγγραφής

dc.creatorMalavaki C.J., Sakkas G.K., Mitrou G.I., Kalyva A., Stefanidis I., Myburgh K.H., Karatzaferi C.en
dc.date.accessioned2023-01-31T08:56:12Z
dc.date.available2023-01-31T08:56:12Z
dc.date.issued2015
dc.identifier10.1007/s10974-015-9439-8
dc.identifier.issn01424319
dc.identifier.urihttp://hdl.handle.net/11615/76175
dc.description.abstractDisuse atrophy is the loss of skeletal muscle mass due to inactivity or lower than ‘normal’ use. It is not only a furtive component of the ‘modern’ sedentary lifestyle but also a part of numerous pathologies, where muscle loss is linked to disease specific and/or other toxicity factors, eventually leading to wasting (cachexia). Whether disuse-or-disease induced, muscle loss leads to weakness and metabolic comorbidities with a high societal and financial cost. This review discusses the intricate network of interacting signalling pathways including Atrogin-1/MAFbx, IGF1-Akt, myostatin, glucocorticoids, NF-kB, MAPKs and caspases that seem to regulate disuse atrophy but also share common activation patterns in other states of muscle loss such as sarcopenia or cachexia. Reactive oxygen species are also important regulators of cell signalling pathways that can accelerate proteolysis and depress protein synthesis. Exercise is an effective countermeasure and antioxidants may show some benefit. We discuss how the experimental model used can crucially affect the outcome and hence our understanding of atrophy. Timing of sampling is crucial as some signalling mechanisms reach their peak early during the atrophy process to rapidly decline thereafter, while other present high levels even weeks and months after study initiation. The importance of such differences lays in future consideration of appropriate treatment targets. Apart from attempting to correct defective genes or negate their effects, technological advances in new rational ways should aim to regulate specific gene expression at precise time points for the treatment of muscle atrophy in therapeutic protocols depending on the origin of atrophy induction. © 2015, Springer International Publishing Switzerland.en
dc.language.isoenen
dc.sourceJournal of Muscle Research and Cell Motilityen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84952949361&doi=10.1007%2fs10974-015-9439-8&partnerID=40&md5=8b5a8cd2aae19ef47f2fa11daca47451
dc.subjectantioxidanten
dc.subjectreactive oxygen metaboliteen
dc.subjectanimalen
dc.subjecthumanen
dc.subjectmetabolismen
dc.subjectmuscle atrophyen
dc.subjectpathologyen
dc.subjectphysiologyen
dc.subjectsignal transductionen
dc.subjectskeletal muscleen
dc.subjectAnimalsen
dc.subjectAntioxidantsen
dc.subjectHumansen
dc.subjectMuscle, Skeletalen
dc.subjectMuscular Atrophyen
dc.subjectMuscular Disorders, Atrophicen
dc.subjectReactive Oxygen Speciesen
dc.subjectSignal Transductionen
dc.subjectSpringer International Publishingen
dc.titleSkeletal muscle atrophy: disease-induced mechanisms may mask disuse atrophyen
dc.typeotheren


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