Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, přehledy
PubMed
35955530
PubMed Central
PMC9368893
DOI
10.3390/ijms23158396
PII: ijms23158396
Knihovny.cz E-zdroje
- Klíčová slova
- intensive care unit-acquired weakness, muscle atrophy, proteostasis, rapamycin system, sarcopenia, ubiquitin–proteasome system,
- MeSH
- jednotky intenzivní péče MeSH
- kosterní svaly MeSH
- kritický stav MeSH
- lidé MeSH
- nemoci svalů * komplikace MeSH
- sarkopenie * komplikace MeSH
- svalová atrofie komplikace MeSH
- svalová slabost etiologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Skeletal muscle is a highly adaptable organ, and its amount declines under catabolic conditions such as critical illness. Aging is accompanied by a gradual loss of muscle, especially when physical activity decreases. Intensive care unit-acquired weakness is a common and highly serious neuromuscular complication in critically ill patients. It is a consequence of critical illness and is characterized by a systemic inflammatory response, leading to metabolic stress, that causes the development of multiple organ dysfunction. Muscle dysfunction is an important component of this syndrome, and the degree of catabolism corresponds to the severity of the condition. The population of critically ill is aging; thus, we face another negative effect-sarcopenia-the age-related decline of skeletal muscle mass and function. Low-grade inflammation gradually accumulates over time, inhibits proteosynthesis, worsens anabolic resistance, and increases insulin resistance. The cumulative consequence is a gradual decline in muscle recovery and muscle mass. The clinical manifestation for both of the above conditions is skeletal muscle weakness, with macromolecular damage, and a common mechanism-mitochondrial dysfunction. In this review, we compare the molecular mechanisms underlying the two types of muscle atrophy, and address questions regarding possible shared molecular mechanisms, and whether critical illness accelerates the aging process.
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