Abstract
Sarcopenia is a common geriatric disorder characterized by decreased muscle strength, low muscle mass and poor physical performance. This aging-related skeletal muscle deterioration leads to adverse outcomes and severely impairs the quality of life of patients. The accumulation of dysfunctional mitochondria with aging is an important factor in the occurrence and progression of sarcopenia. Mitochondrial quality control (MQC) fundamentally ensures the normal mitochondrial functions and is comprised of four main parts: proteostasis, biogenesis, dynamics and autophagy. Therefore, any pathophysiologic factors compromising the quality control of homeostasis in the skeletal muscle may lead to sarcopenia. However, the specific theoretical aspects of these processes have not been fully elucidated. Current therapeutic interventions using nutritional and pharmaceutical treatments show a modest therapeutic efficacy; however, only physical exercise is recommended as the first-line therapy for sarcopenia, which can ameliorate skeletal muscle deficiency by maintaining the homeostatic MQC. In this review, we summarized the known mechanisms that contribute to the pathogenesis of sarcopenia by impairing normal mitochondrial functions and described potential interventions that mitigate sarcopenia through improving MQC.
Highlights
Senescence is a natural process of aging associated with degeneration of physical functions
We summarized the potential mechanisms of mitochondrial dysfunction with an emphasis on promising therapeutic interventions to prevent and ameliorate sarcopenia during aging
In the skeletal muscle of senescence-accelerated mouse (SAM) prone 8 (SAMP8), a canonical sarcopenia model, protein synthesis-related markers (Akt, mTOR and p70S6K) were reduced; the protein degradation-associated markers (FoxO3, MuRF-1 and Muscle Atrophy F-box (MAFbx)) were elevated indicating during advancing process of aging, protein turnover has a pro-degradation trend that leads to muscle atrophy which contributes to the occurrence of sarcopenia [55]
Summary
Senescence is a natural process of aging associated with degeneration of physical functions. The gradual loss of muscle mass, strength and function is one of the most important hallmarks of aging. The loss of muscle mass probably reaches 1 to 2% per year from 50 to 60 years and 3% to 5% per year at older ages [1]. In 2019, the European Working Group on Sarcopenia in Older People 2 (EWGSOP2) launched the latest diagnostic criteria for sarcopenia, including low muscle strength, decreased muscle quantity/quality or poor. An increasing number of studies have indicated that dysfunctional mitochondria may play a central role in the pathogenesis of sarcopenia. Adverse alternations in the quality control mechanisms may lead to mitochondrial dysfunction, which can further contribute to muscle wasting and even sarcopenia [22,23,24,25]. We summarized the potential mechanisms of mitochondrial dysfunction with an emphasis on promising therapeutic interventions to prevent and ameliorate sarcopenia during aging
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