Cellular and molecular mechanisms of sarcopenia: the S100B perspective

Abstract

Primary sarcopenia is a condition of reduced skeletal muscle mass and strength, reduced agility, and increased fatigability and risk of bone fractures characteristic of aged, otherwise healthy people. The pathogenesis of primary sarcopenia is not completely understood. Herein, we review the essentials of the cellular and molecular mechanisms of skeletal mass maintenance; the alterations of myofiber metabolism and deranged properties of muscle satellite cells (the adult stem cells of skeletal muscles) that underpin the pathophysiology of primary sarcopenia; the role of the Ca2+‐sensor protein, S100B, as an intracellular factor and an extracellular signal regulating cell functions; and the functional role of S100B in muscle tissue. Lastly, building on recent results pointing to S100B as to a molecular determinant of myoblast–brown adipocyte transition, we propose S100B as a transducer of the deleterious effects of accumulation of reactive oxygen species in myoblasts and, potentially, myofibers concurring to the pathophysiology of sarcopenia.

Age- and sex-specific effects in paravertebral surface electromyographic back extensor muscle fatigue in chronic low back pain

“…On the muscle cell function level, a blunted protein production in aged muscles is caused by impaired anabolic signaling of the peroxisome proliferatoractivated receptor-ɣ coactivator-1α (PGC-1α)-a key regulator of mitochondrial biogenesis-which may reduce sensitivity to insulin and impair the expression of Akt and mammalian target of rapamycin (mTOR). In parallel, increased muscle protein degradation via the calpain and the autophagy pathways (rather than the ubiquitin proteasome pathway) takes place (Riuzzi et al 2018). Loss of muscle endurance and strength is related to deficiencies within the respiratory chain due to a decline in both the number and function of mitochondria (Joseph et al 2016).…”

Comprehensive analysis of skeletal muscle- and bone-derived mesenchymal stem/stromal cells in patients with osteoarthritis and femoral neck fracture

“…Age-related OP is commonly accompanied by sarcopenia, a condition that is characterized by muscle weakness, muscle fiber atrophy, and adipose tissue infiltration into muscle [10,11]. Although the precise cause of sarcopenia remains unknown, it has been proposed that a combination of factors are involved, including systemic inflammation, increased oxidative stress, and changes in skeletal muscle stem cell populations [12][13][14].…”

Sarcopenia in Older Adults

“…This section will include, in brief, the most common mechanisms related to sarcopenia: oxidative stress [reactive oxygen and nitrogen species (ROS and RNS)]; a-without clinical symptoms of muscle fiber inflammation (due to presence of myokines/cytokines like TNF-α and IL-6); hormonal regulation impairment (such as testosterone, growth hormone, IGF-1, glutathione 4, insulin resistance, and vitamin D); vitamin E deficiency; proteolysis pathway [the lack of responsiveness of the ubiquitinproteasome system and alterations in the regulation of autophagy and apoptotic pathway (Bcl2 signaling and NF-Kb)]; and finally, the role of adult stem (satellite) cells. Identifying these mechanisms and their underlying origins is expected to facilitate strategy of intervention programs [28].…”