2022
DOI: 10.1016/j.redox.2022.102398
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Fast regulation of the NF-κB signalling pathway in human skeletal muscle revealed by high-intensity exercise and ischaemia at exhaustion: Role of oxygenation and metabolite accumulation

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Cited by 13 publications
(10 citation statements)
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“…The factors that affect the percentage of protein utilization during exercise include training status, exercise intensity, and the availability of other substrates (e.g., carbohydrates). From a molecular basis, it was reported that endurance exercise reduces the activation of nuclear factor-κ, leading to mitochondrial adaptations that prevent protein degradation [ 42 ]. The substrate utilization in this study depends on the respiratory quotation (RQ) that the IC calculates.…”
Section: Discussionmentioning
confidence: 99%
“…The factors that affect the percentage of protein utilization during exercise include training status, exercise intensity, and the availability of other substrates (e.g., carbohydrates). From a molecular basis, it was reported that endurance exercise reduces the activation of nuclear factor-κ, leading to mitochondrial adaptations that prevent protein degradation [ 42 ]. The substrate utilization in this study depends on the respiratory quotation (RQ) that the IC calculates.…”
Section: Discussionmentioning
confidence: 99%
“…While the precise contribution of NF-κB signaling to the baseline gene expression pattern remains elusive, in the exercising muscle, we clearly could depict NF-κB together with the TF HIF1α as being among the major drivers of the acute exercise-provoked transcriptional stress response, both in SED as well as in ET individuals, as illustrated by a significant enrichment of related pathways in the exercise-provoked gene signatures. Both TFs have previously been shown to become activated in skeletal muscle during acute exercise, accumulate in the nucleus, and associate with chromatin at their target sites [ 51 , 74 , 75 ]. Moreover, there is increasing evidence that these two signaling pathways are intimately linked and coordinately act together in shaping exercise-provoked myofibrillar stress signaling to cope with acute shortages in energy and oxygen supplies, accumulation of reduced oxygen intermediates, perturbations in intracellular calcium levels, enforced mechanical strain at the contractile apparatus, and increased release of stress hormones [ 75 , 76 , 77 ].…”
Section: Discussionmentioning
confidence: 99%
“…Цьому також сприяє здатність піролідиндиотіокарбамату амонію та диметилфумарату зменшувати метаболічні розлади, спричинені гіпомелатонінемією і ВЛД, зокрема інсулінорезистентність та дисліпопротеїнемію [13,14], які, як відомо, також сприяють виробленню АФК і АФА та прозапальних цитокінів [28]. Надмірна активація NF-κB виявляється особливо небезпечною для функціонування скелетних м'язів, наслідком чого є порушення їх скоротливості та атрофія [29], розвиток інсулінорезистентності [30].…”
Section: результати та їх обговоренняunclassified