Sarcopenia – Molecular mechanisms and open questions

• Published in: Ageing research reviews Vol. 65; p. 101200
• Main Authors: Wiedmer, Petra, Jung, Tobias, Castro, José Pedro, Pomatto, Laura C.D., Sun, Patrick Y., Davies, Kelvin J.A., Grune, Tilman
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 01.01.2021
• Subjects: Aging; Autophagy; Humans; Mitochondria, Muscle fibre composition; Molecular pathways; Muscle, Skeletal - pathology; Muscular Atrophy - pathology; Proteasome; Proteostasis; Quality of Life; Sarcopenia - pathology; Molecular pathways; Proteostasis; Mitochondria, Muscle fibre composition; Autophagy; Proteasome
• ISSN: 1568-1637; 1872-9649
• DOI: 10.1016/j.arr.2020.101200

•Sarcopenia, a muscle-wasting syndrome during normal aging, is mainly characterized by loss of muscle strength and mass.•Several molecular mechanisms have been described as causes for sarcopenia.•Main mechanisms represent loss of proteostasis, mitochondrial dysfunction and inflammatory disturbances.•Open questions consider the role of muscular fat infiltration, fibre-specific regulation and therapeutic impact of the diet. Sarcopenia represents a muscle-wasting syndrome characterized by progressive and generalized degenerative loss of skeletal muscle mass, quality, and strength occurring during normal aging. Sarcopenia patients are mainly suffering from the loss in muscle strength and are faced with mobility disorders reducing their quality of life and are, therefore, at higher risk for morbidity (falls, bone fracture, metabolic diseases) and mortality. Several molecular mechanisms have been described as causes for sarcopenia that refer to very different levels of muscle physiology. These mechanisms cover e. g. function of hormones (e. g. IGF-1 and Insulin), muscle fiber composition and neuromuscular drive, myo-satellite cell potential to differentiate and proliferate, inflammatory pathways as well as intracellular mechanisms in the processes of proteostasis and mitochondrial function. In this review, we describe sarcopenia as a muscle-wasting syndrome distinct from other atrophic diseases and summarize the current view on molecular causes of sarcopenia development as well as open questions provoking further research efforts for establishing efficient lifestyle and therapeutic interventions.