Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1287503 | ENA |
REPOSITORIES: ENA
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Project description:We previously reported that skeletal muscle adaptation to regular exercise requires a healthy gut microbiome, contributing to growing evidence that some exercise benefits are mediated by microbiome-derived metabolites. Here, to identify such exercise-associated microbial metabolites, we transfer cecal contents from exercise-trained donor mice into exercise-naïve recipient mice undergoing unilateral hindlimb immobilization. Recipients of cecal material from exercise-trained donors exhibit less muscle atrophy compared with those receiving transfers from sedentary donors. Untargeted metabolomics reveal metabolites enriched in cecal content, serum, and muscle of recipients from exercise-trained donors, consistent with microbial origin. Oral administration of two such metabolites (pipecolic acid and succinate) attenuates muscle atrophy and preserves muscle function in exercise-naïve mice, potentially by enhancing cellular energy status and translational capacity. These findings further define the gut microbiome-skeletal muscle axis and provide evidence that exercise-associated microbial metabolites serve as a novel class of exercise mimetics for treating conditions responsive to physical activity.
2026-05-27 | PXD077599 | Pride
Project description:Muscle atrophy is a morbidity and mortality risk factor that happens with disuse, chronic disease, and ageing. Recovery from atrophy involves changes in protein synthesis and different cell types such as muscle fibers, and satellite and immune cells. Here we show that the previously uncharacterized gene and protein Zfp697 is a damage-induced regulator of muscle regeneration. Zfp697/ZNF697 expression is transiently elevated during recovery from muscle atrophy or injury in mice and humans. Sustained Zfp697 expression in mouse muscle leads to a gene expression signature of chemokine secretion, immune cell recruitment, and extracellular matrix remodeling. Myofiber-specific Zfp697 ablation hinders the inflammatory and regenerative response to muscle injury, compromising functional recovery. We uncover Zfp697 as an essential mediator of the interferon gamma response in muscle cells that functions primarily as an ncRNA-binding protein, most notably the pro-regenerative miR-206. This work identifies Zfp697 as an integrator of cell-cell communication necessary for tissue regeneration.
2024-07-30 | GSE273094 | GEO
Project description:Loss of muscle mass and strength following disuse followed by impaired muscle recovery likely contribute to sarcopenia in older adults. Metformin and leucine individually have shown positive effects in skeletal muscle during atrophy conditions but have not been evaluated in combination nor under the conditions of disuse atrophy and recovery in aging. The purpose of this study was to determine if a dual treatment of metformin and leucine (MET+LEU) would prevent disuse-induced atrophy and/or promote muscle recovery in aged mice (22-24 mo). We were also interested if these muscle responses correspond to changes in satellite cells and ECM abundance. Aged mice were subjected to 14 days of hindlimb unloading (HU) followed by 7 or 14 days of reloading (7 or 14d RL). Metformin (MET), leucine (LEU), or MET+LEU was administered via drinking water and were compared to Vehicle-treated mice. We observed that MET+LEU increased whole body grip strength, muscle specific force and satellite cell abundance during HU but did not alter muscle size during HU or RL. Moreover, MET+LEU treatment increased ECM turnover driven by a decrease in collagen IV content during 7 and 14d RL. Transcriptome analysis revealed that MET+LEU altered Gene Set Enrichment Analysis hallmark pathways related to inflammation and myogenesis during HU. Together , MET+LEU was able to improve muscle quality during disuse and recovery in aging possibly by increasing muscle satellite cell content and reducing excessive ECM accumulation.
2021-09-01 | GSE167462 | GEO
Project description:Cancer cachexia is a multifactorial wasting syndrome affecting body and lean tissue mass that is often exacerbated by anticancer chemotherapy. In this study, we used a mouse model of acute myeloid leukemia chemotherapy induction regimen (CIR) comprising daunorubicin and cytarabine to investigate the molecular mechanisms underlying cachexia. Quantitative tandem mass tag (TMT) based proteomics was performed on skeletal muscle (quadriceps) to uncover biomarkers and pathways associated with chemotherapy induced muscle wasting. Our findings demonstrate that the AML CIR induced an acute cachexic phenotype characterized by approximately 10 percent body and lean mass loss and 20 percent muscle fibre atrophy. Through deep proteome profiling, two potential biomarkers—haptoglobin (Hp) and glutamine synthetase (Glul)—were identified. Haptoglobin in particular was responsive to cachexia severity, recovery, and exacerbation via exercise, indicating its potential as a conditionally sensitive biomarker of muscle wasting. Pathway analysis revealed upregulation of mitochondrial metabolism including branched chain amino acid catabolism and mitochondrial uncoupling proteins (Ucp1 and Ucp3), suggesting hypermetabolism as a key driver of the phenotype. These data support the use of skeletal muscle proteomics in characterizing chemotherapy induced cachexia and identifying sensitive muscle specific biomarkers for future translational and therapeutic studies.
2025-06-16 | PXD063910 | Pride
Project description:Secondary muscle atrophy due to neuronal denervation is a key determinant of poor functional recovery in immune-mediated neuropathies, even after resolution of inflammation. Activin II receptors (ActIIRs) are central mediators of muscle atrophy, and their inhibition has shown variable efficacy in primary myopathies. We investigated the therapeutic potential of ActIIR inhibition in promoting motor recovery in immune-mediated neuropathies using the experimental autoimmune neuritis (EAN) model in Lewis rats. Motor performance was evaluated through a composite of clinical neuritis scoring, grip strength testing, and balance beam performance combined with kinematic gait analysis. High-dose antibody treatment significantly improved motor outcome. This improvement was not associated with changes in peripheral nerve inflammation or remyelination but correlated with preservation of muscle fiber size. Muscle proteomic analysis revealed modulation of the FoxO signaling pathway and reduced expression of the atrophy-related E3 ligases Atrogin-1 and MuRF1. These findings indicate that ActIIR inhibition prevents secondary muscle atrophy and enhances motor recovery in autoimmune neuritis. Targeting ActIIR signaling may represent a promising therapeutic strategy to improve motor outcomes in patients with immune-mediated neuropathies.
2026-04-13 | PXD070456 | Pride
Project description:We performed gene expression microarray analysis of skeletal muscle biopsies from normal glucose tolerant subjects and type 2 diabetes subjects obtained during a 60 min bicycle ergometer exercise and the 180 min of recovery phase We analysed skeletal mucle biopsies from patients with T2D and from control subjects (n=7 each) at three time points during exercise and recovery
2015-07-03 | E-GEOD-59363 | biostudies-arrayexpress
Project description:Muscle atrophy is a morbidity and mortality risk factor that happens with disuse, chronic disease, and ageing. Recovery from atrophy involves changes in protein synthesis and different cell types such as muscle fibers, and satellite and immune cells. Here we show that the previously uncharacterized gene and protein Zfp697 is a damage-induced regulator of muscle regeneration. Zfp697/ZNF697 expression is transiently elevated during recovery from muscle atrophy or injury in mice and humans. Sustained Zfp697 expression in mouse muscle leads to a gene expression signature of chemokine secretion, immune cell recruitment, and extracellular matrix remodeling. Myofiber-specific Zfp697 ablation hinders the inflammatory and regenerative response to muscle injury, compromising functional recovery. We uncover Zfp697 as an essential mediator of the interferon gamma response in muscle cells that functions primarily as an ncRNA-binding protein, most notably the pro-regenerative miR-206. This work identifies Zfp697 as an integrator of cell-cell communication necessary for tissue regeneration.
2024-07-30 | GSE273093 | GEO
Project description:Muscle atrophy is a morbidity and mortality risk factor that happens with disuse, chronic disease, and ageing. Recovery from atrophy involves changes in protein synthesis and different cell types such as muscle fibers, and satellite and immune cells. Here we show that the previously uncharacterized gene and protein Zfp697 is a damage-induced regulator of muscle regeneration. Zfp697/ZNF697 expression is transiently elevated during recovery from muscle atrophy or injury in mice and humans. Sustained Zfp697 expression in mouse muscle leads to a gene expression signature of chemokine secretion, immune cell recruitment, and extracellular matrix remodeling. Myofiber-specific Zfp697 ablation hinders the inflammatory and regenerative response to muscle injury, compromising functional recovery. We uncover Zfp697 as an essential mediator of the interferon gamma response in muscle cells that functions primarily as an ncRNA-binding protein, most notably the pro-regenerative miR-206. This work identifies Zfp697 as an integrator of cell-cell communication necessary for tissue regeneration.
2024-07-30 | GSE273092 | GEO
Project description:This study investigates the effects of aerobic exercise on skeletal muscle atrophy in CT26 tumor-bearing mice through transcriptomic and weighted gene co-expression network analyses.
2026-04-16 | GSE328094 | GEO
Project description:Disuse-induced muscle atrophy commonly occurs following illness, injury, or falls and becomes increasingly frequent with ageing. Whether skeletal muscle retains a “memory” of repeated disuse remains unknown. We investigated repeated lower- limb immobilization in young adults and a refined aged rat model, integrating physiological, multi-omic, immunohistochemical, biochemical, and primary human muscle stem cell (MuSC) analyses. To enable robust age comparisons, we integrated previously published young rat data with newly generated aged rat data. In young human muscle, repeated disuse elicited attenuated transcriptional perturbations in oxidative and mitochondrial pathways, suggestive of a protective molecular memory, despite similar atrophy to initial disuse. In contrast, aged muscle exhibited a detrimental memory, characterized by greater atrophy, exaggerated suppression of aerobic metabolism genes despite recovery after initial disuse, NAD+ and mitochondrial DNA depletion, and activation of proteasomal, extracellular-matrix, and DNA-damage pathways. Whereas young rats recovered muscle mass after initial disuse, aged rats failed to do so. Across species, repeated disuse induced DNA hypermethylation and downregulation of aerobic metabolism and mitochondrial gene networks. NR4A1 and NR4A3 were among the strongest disuse- suppressed genes; NR4A1 acquired recovery-phase hypermethylation that maintained its transcriptional repression, while NR4A3 was the most downregulated gene after initial atrophy and remained persistently suppressed into recovery. Acetylcholine receptor subunit genes (CHRNA1, CHRND) were epigenetically primed, demonstrating hypomethylation and strong upregulation after disuse, and further amplification after repeated atrophy, while CHRNG was selectively induced after repeated atrophy only. NMRK2, an NAD+ biosynthesis gene, was the most downregulated gene across both atrophy periods, and supplementation with its substrate, nicotinamide riboside (NR), improved myotube size in MuSCs derived post-atrophy. Overall, repeated disuse atrophy imprints a molecular memory in skeletal muscle shaping transcriptional resilience in young adults and exaggerated susceptibility in aged muscle.
2026-02-24 | GSE310849 | GEO