![]() They found 73 genes with altered expression, with increased expression of genes involved in inflammation and immune response, and consistent with Zahn et al. In this cross-species, cross-platform analysis, gene orthologues were meta-analyzed for approximately 400 samples, 42 of which were from human skeletal muscle, comparing old to young individuals. ![]() De Magalhaes and colleagues conducted a meta-analysis of microarray experiments on aging in mice, rats, and humans across a variety of tissues. described a 250-gene signature for muscle aging, compared this to age-associated gene regulation in other tissues and found increased expression of pathways regulating cell growth, complement activation, and ribosomal and extracellular matrix genes and decreased expression of genes for chloride transport and mitochondrial oxidative phosphorylation (OXPHOS). In one of the largest previous studies on gene expression in aging muscle, muscle biopsies from 81 individuals were investigated. In order to efficiently delay the onset and severity of sarcopenia, it is crucial to more in detail describe the molecular mechanisms causing this physiological deterioration of muscle function. This indicates that sarcopenia is not only a matter of loss of muscle mass but rather a concomitant loss of muscle mass and a decline of muscle quality. As we age, we lose approximately 1 % of leg lean mass per year and approximately 2.5–4 % in leg strength, men to a higher extent than women. This condition, often termed age-related sarcopenia, leads to a variety of physical conditions that reduce life quality and overall health in aging individuals. These results support that mitochondrial dysfunction is a major age-related factor and also highlight the beneficial effects of maintaining a high physical capacity for prevention of age-related sarcopenia.Īging profoundly affects skeletal muscle, including loss of muscle mass and strength and increasing the levels of fat and connective tissue. Strikingly, 20 out of those 21 genes are regulated in opposite direction when comparing increasing age with increasing VO 2MAX. Out of the 957 genes associated with aging, 21 ( p < 0.001, false discovery rate = 5 %, n = 116) were also associated with maximal oxygen consumption (VO 2MAX). ![]() We also discover genes previously not linked to muscle aging and metabolism, such as fasciculation and elongation protein zeta 2 (FEZ2, p = 2.8 × 10 −8). Among the genes with the strongest association with aging were H3 histone, family 3B (H3F3B, p = 3.4 × 10 −13), AHNAK nucleoprotein, desmoyokin (AHNAK, p = 6.9 × 10 −12), and histone deacetylase 4 (HDAC4, p = 4.0 × 10 −9). Aging was associated with perturbation of many central metabolic pathways like mitochondrial function including reduced expression of genes in the ATP synthase, NADH dehydrogenase, cytochrome C reductase and oxidase complexes, as well as in glucose and pyruvate processing. We find 957 genes to be significantly associated with aging ( p < 0.05, FDR = 5 %, n = 361). Using this data set, we aimed to elucidate the molecular mechanism of muscle aging and to describe how physical exercise may alleviate negative physiological effects. The created muscle compendium is a publicly available resource including all curated annotation. To address these issues, we have performed a complete re-annotation of public microarray data from human skeletal muscle biopsies and constructed a muscle expression compendium consisting of nearly 3000 samples. Although high-throughput studies of gene expression have generated large amounts of data, most of which is freely available in public archives, the use of this valuable resource is limited by computational complications and non-homogenous annotation.
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