Purpose: A short period of disuse of 1-2 weeks due to factors such as illness or injury can lead to muscle atrophy, affecting both athletic performance and health. Recent research has shown that uridine 5'-monophosphate (5'-UMP) can counteract disuse-induced muscle atrophy by increasing PGC-1α expression and inhibiting atrogin-1 expression. However, the effect of 5'-UMP on disuse muscle atrophy in humans remains unknown.
View Article and Find Full Text PDFRespiratory syncytial virus (RSV) is a leading cause of upper and lower respiratory tract infection, especially in children and the elderly. Various vaccines containing the major transmembrane surface proteins of RSV (proteins F and G) have been tested; however, they have either afforded inadequate protection or are associated with the risk of vaccine-enhanced disease (VED). Recently, F protein-based maternal immunization and vaccines for elderly patients have shown promising results in phase III clinical trials, however, these vaccines have been administered by injection.
View Article and Find Full Text PDFAtrogin-1 and muscle RING finger 1 (MuRF1) are ubiquitin ligases specifically expressed during skeletal muscle atrophy and mediate muscle protein degradation. In contrast, PGC-1α (peroxisome proliferator-activated receptor γ coactivator 1α), which is a master regulator of mitochondrial biosynthesis, protects skeletal muscle from atrophy. Pyrimidine nucleoside 5'-monophosphates, such as cytidine 5'-monophosphate (5'-CMP) and uridine 5'-monophosphate (5'-UMP), induce PGC-1α expression and promote myotube formation in mouse C2C12 cells.
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