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Icariin Ameliorates Exercise-Induced Fatigue by Promoting TFEB-Dependent Mitochondrial Clearance and Metabolic Re-programming

ABSTRACT: Icariin Ameliorates Exercise-Induced Fatigue by Promoting TFEB-Dependent Mitochondrial Clearance and Metabolic Re-programming, which reveals a novel molecular mechanism underlying icariin’s anti-fatigue efficacy and highlights its potential as a natural agent for enhancing exercise capacity.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE313438 | GEO | 2025/12/16

REPOSITORIES: GEO

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Lcariin Ameliorates Exercise-Induced Fatigue by Promoting TFEB-Dependent Mitochondrial Clearance and Metabolic Re-programming

Project description:Lcariin Ameliorates Exercise-Induced Fatigue by Promoting TFEB-Dependent Mitochondrial Clearance and Metabolic Re-programming, which reveals a novel molecular mechanism underlying icariin’s anti-fatigue efficacy and highlights its potential as a natural agent for enhancing exercise capacity.

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Physical activity diminish fatigue and systemic interferon response in multiple sclerosis

Project description:Objective: To evaluate gene expression profiles in multiple sclerosis (MS) patients who improved their fatigue status after a program of physical exercise and to compare them with healthy controls (HC). Methods: A prospective longitudinal study was conducted. Gene expression in whole blood was profiled at baseline in 7 healthy controls and also in 7 fatigued-MS patients. Patients underwent a physical exercise program for 6 months, and their fatigue status and gene expression profiles were again analyzed at the end of this program. Results: MS patients showed a significant activation of genes participating in the systemic interferon response in comparison with healthy controls. Fatigue improved at the end of the physical activity program, and, in parallel, systemic activation of interferon related genes disappeared. Conclusions: Fatigue improvement following an exercise program is associated to down modulation of interferon activity at the systemic level in MS patients. Our results provide a biological basis for the observed benefit of physical exercise in MS.

2015-09-27 | E-MTAB-2973 | biostudies-arrayexpress

Project description:Icariin Ameliorates Exercise-Induced Fatigue by Promoting TFEB-Dependent Mitochondrial Clearance and Metabolic Re-programming

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Expression data from injected mice overexpressing TFEB specifically in liver

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DNA Methylation Patterns Associated with Fatigue in Primary SjÃ¶grenâs Syndrome

Project description:Genome-wide analysis of DNA methylation profiles from patients with SjÃ¶gren's syndrome with high versus low fatigue levels using the Illumina Infinium HumanMethylation450 Beadchip array. Background Chronic fatigue is a common, disabling, and poorly understood phenomenon. Recent studies indicate that epigenetic mechanisms may be involved in the expression of fatigue, a prominent feature of primary SjÃ¶grenâs syndrome (pSS). The aim of this study was to investigate whether DNA methylation profiles of whole blood are associated with fatigue in patients with pSS. Methods 48 pSS patients with high (n=24) or low (n=24) fatigue as measured by a visual analogue scale were included. Genome-wide DNA methylation was investigated using the Illumina HumanMethylation450 BeadChip array. Case-case study including SjÃ¶gren's patients with high fatigue (n=24) and patients with low fatigue levels (n=24)

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DNA Methylation Patterns Associated with Fatigue in Primary Sjögren’s Syndrome

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Project description:Our studies in Salmonella Typhimurium (S. Typhimurium)-infected cells indicate that TFEB has a non-transcriptional, cytosolic function in addition to its well-characterized role as a transcription factor in regulating autophagy and lysosome biogenesis. An unbiased proteomics approach revealed that TFEB interacts with several mitochondrial proteins, which is lost when infected with S. Typhimurium. Microscopical and biochemical examinations further confirmed a novel localization of TFEB in mitochondria. We have also identified a TOMM20 binding motif within the protein sequence of TFEB which, facilitates the mitochondrial translocation in a mTOR-dependent manner. Our results further demonstrate that TFEB and the mitochondrial protease LonP1 co-regulate the assembly of complex I and its function. Moreover, during S. Typhimurium infection, lack of TFEB specifically in the mitochondria exacerbates the expression of pro-inflammatory cytokines.

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Gene expression analysis of cancer-related fatigue in whole blood from breast cancer survivors

Project description:Cancer-related fatigue is one of the most frequent complaints among breast cancer survivors, with a major negative impact on general life. However, the etiology behind this syndrome is still unraveled. Gene expression analysis was performed on whole blood samples from breast cancer survivors classified as either fatigued or non-fatigued at two consecutive time points. The analysis identified several gene sets concerning plasma and B cell pathways as different between the fatigue and non-fatigue groups, suggesting that a deregulation in these pathways might underlie the fatigue syndrome. The fatigue group also showed a higher mean level of leucocytes, lymphocytes and neutrophiles compared with the non-fatigue group, thus further implicating the immune system in the biology behind the fatigue syndrome. Keywords: Blood RNA and late side effects Breast cancer survivors treated with adjuvant radiotherapy at The Norwegian Radium Hospital between 1998 and 2002 were invited to participate in a study assessing late treatment effects in breast cancer survivors. In the present study, gene expression analysis was performed on whole blood samples from breast cancer survivors with and without persistent fatigue, to look for different expression patterns that might shed light on the biology behind cancer-related fatigue.

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