PMC:7601109 / 51522-52961 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7601109","sourcedb":"PMC","sourceid":"7601109","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7601109","text":"Skeletal muscle tissues represent the largest protein store in the human body (30–45% of total protein). Muscular mass, strength, and functions are greatly governed by the rates of muscle protein synthesis and turnover [124]. Muscle protein metabolism is regulated by the interaction of a wide range of genes. Aging is associated with various stresses, which increase the expression of catabolic genes such as E3 ubiquitin ligases MuRF1 and atrogin-1 (MAFbx). These genes heighten the occurrence of age-related muscular atrophy [97]. Oral consumption of royal jelly by aged HET mice resulted in lower levels of catabolic genes (e.g., MuRF1 and MAFbx), which were similar to those in young mice. In the meantime, the expression of these genes in the control mice was high indicating that royal jelly can delay age-related muscular apoptosis by suppressing the activity of catabolic genes [97]. Two other studies reported that CAPE suppressed catabolism that contributed to degenerative myopathy in the gastrocnemius muscle of rats undergoing eccentric exercising or femoral artery ligation as reflected by decreased serum levels of creatine kinase, a marker of muscular proteolysis [101,102,103]. Apart from skeletal muscle, CAPE was reported to protect heart muscle against age-related deteriorations such as accumulation of lipofuscin, nuclear irregularity, mitochondrial degeneration, and myofilament disorganization and disruption 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