Biological Aging of Human Skeletal Muscle
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA728322 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14471200.fastq.gz | Fastqsanger.gz | |||
| SRR14471201.fastq.gz | Fastqsanger.gz | |||
| SRR14471202.fastq.gz | Fastqsanger.gz | |||
| SRR14471203.fastq.gz | Fastqsanger.gz | |||
| SRR14471204.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 72 |
Similar Datasets
Project description:The age-related loss of skeletal muscle mass and function (sarcopenia) is one of the most dramatic changes affecting the human body. A clear understanding of the mechanisms involved is thus of paramount importance in ensuring quality of life in the old age. Most previous studies of sarcopenia in human investigated chronological aging, as they relied on comparisons between young and old subjects. Notably, no previous study has taken into consideration inter-individual differences (biological aging) in prevalence of sarcopenia. To obtain an integrative view of muscle biological aging our project uses a single biopsy from 72 well-phenotyped 80 years healthy subjects with different muscle loss/gain (PROOF cohort), to provide an extended characterization of the muscle tissue, including microstructural and omic analyses.
2024-05-02 | GSE174106 | GEO
Project description:Ribosome profiling analysis of aging human skeletal muscle
| PRJNA639710 | ENA
Project description:Skeletal muscle aging is a major causative factor for disability and frailty in the elderly. Recent theories about the origins of the progressive impairment of skeletal muscle with aging emphasize a disequilibrium between damage and repair. Macrophages participate in muscle tissue repair first as pro-inflammatory M1 subtype and then as M2 anti-inflammatory subtype. However, information on macrophage presence in skeletal muscle is still sporadic and the effect of aging on different phenotypes remains unknown. In this study, we sought to characterize the polarization status of macrophages human skeletal muscle at different ages. We found that most macrophages in human skeletal muscle are M2, and that this number increased with advancing age. On the contrary, M1 macrophages decline with aging, making the total number of macrophages invariant with older age. Notably, M2 macrophages co-localized with increasing intermuscular adipose tissue (IMAT) in aging skeletal muscle. The mouse strain BALB/c, intrinsically M2-prone, showed increased IMAT and regenerating myofibers in skeletal muscle, accompanied by elevated expression of adipocyte markers and M2 cytokines. Collectively, we report that polarization of macrophages to the major M2 subtype is associated with IMAT, and propose that increased M2 in aged skeletal muscle may reflect active repair of aging-associated muscle damage.
2022-01-01 | GSE125481 | GEO
Project description:Exercise Mitigates Skeletal Muscle Epigenetic Aging
| PRJNA732356 | ENA
Project description:Skeletal Muscle Transcriptome in Healthy Aging
| PRJNA690800 | ENA
Project description:A common characteristic of aging is the loss of skeletal muscle (sarcopenia) which can lead to falls and fractures. MicroRNAs (miRNA) are novel post-transcriptional modulators of gene expression with a potential role as a regulator of skeletal muscle mass and function. The purpose of this study was to profile miRNA expression patterns in aging human skeletal muscle using a miRNA array followed by in-depth functional and network analysis. Muscle biopsy samples from 36 men (young: 31±2; n=19; older: 73±3; n=17) were: 1) analyzed for the expression of miRNAs using a microRNA array 2) validated with Taqman quantitative real-time PCR assays, and 3) identified (and later validated) for potential gene targets using the bioinformatics knowledge base software, Ingenuity Pathways Analysis. We found that 18 miRNAs were differentially expressed in older humans (P<0.05 and >500 expression level). The Let-7 family members, Let-7b and Let-7e, were significantly elevated and further validated in older subjects (P<0.05). Functional and network analysis from Ingenuity determined that gene targets of the Let-7’s were associated with molecular networks involved in cell cycle control such as cellular proliferation and differentiation. We confirmed with real-time PCR that the mRNA expression of the cell cycle regulators, CDK6, CDC25A and CDC34 were downregulated in older subjects compared to the young (P<0.05). These data suggest that aging is characterized by an increased expression of Let-7 family members which may downregulate genes related to cellular proliferation. We propose that the increased Let-7 expression in older human muscle may be an indicator of impaired cell cycle function.
2010-10-01 | GSE23527 | GEO
Project description:Ribosome profiling analysis of aging human skeletal muscle (RNA-Seq)
| PRJNA639715 | ENA
Project description:Ribosome profiling analysis of aging human skeletal muscle (Ribo-Seq)
| PRJNA639716 | ENA
Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging
2007-07-16 | GSE8479 | GEO
Project description:Human skeletal muscle transcriptome
| PRJNA412170 | ENA