Abstract
Skeletal muscle aging is associated with a significant loss of skeletal muscle strength and power (i.e., dynapenia), muscle mass and quality of life, a phenomenon known as sarcopenia. This condition affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in geriatric patients. Notwithstanding the exact mechanisms responsible for sarcopenia are not fully understood, mitochondria have emerged as one of the central regulators of sarcopenia. In fact, there is a wide consensus on the assumption that the loss of mitochondrial integrity in myocytes is the main factor leading to muscle degeneration. Mitochondria are also key players in senescence. It has been largely proven that the modulation of mitochondrial functions can induce the death of senescent cells and that removal of senescent cells improves musculoskeletal health, quality, and function. In this review, the crosstalk among mitochondria, cellular senescence, and sarcopenia will be discussed with the aim to elucidate the role that the musculoskeletal cellular senescence may play in the onset of sarcopenia through the mediation of mitochondria.
Highlights
Declines in skeletal muscle mass and function are among the most notable corollary of aging
The aging process is caused by cumulative oxidative damage to cells by free radicals Superoxide dismutase is an antioxidant defense against superoxide, the origin of most reactive oxygen species (ROS) Oxidative stress is defined as an excessive accumulation of pro-oxidative features and ROS
Mitochondria is the main source of free radicals and the key target for oxidative damage Oxidative damage does not correlate with chronological age but rather with their frailty state
Summary
Declines in skeletal muscle mass and function are among the most notable corollary of aging. The term sarcopenia was coined by Rosenberg [3] from the Greek words “sarx” (flesh) and “penia” (poverty) to describe the loss of muscle mass with aging. This condition affects nearly one-third of the older population [2], and is one of the main factors leading to negative health outcomes in older adults [4]. Other factors that contribute to muscle loss in advanced age include neuromuscular junction dysfunction, reduced satellite cell number/function, decreased number of motor units [17], intramuscular adipose tissue infiltration [18], inflammation [19], insulin resistance [20], mitochondrial dysfunction [21], and oxidative stress [22]. We illustrate the involvement of mitochondria in cellular senescence with the aim to highlight the relationship between musculoskeletal cellular senescence induced by mitochondrial dysfunction and the onset of sarcopenia
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