Abstract
Simple SummaryWith old age, the strength and size of our muscles worsens with time, affecting our ability to carry out daily activities. Muscle wasting may be more dangerous for some people, causing falls, inactivity, and a loss of self-sufficiency. This severe muscle-wasting condition is called sarcopenia. Mitochondria are sub-cellular organelles involved in the regulation of determinant functions in muscles, such as energy production and programmed cell death. The present review describes muscle modifications and mitochondria alterations occurring in old age, digesting the most important discoveries on mitochondrial changes in sarcopenia. Our comprehensive summary of scientific advances in this field during the last years will be of help for researchers to design future investigations which clarify further aspects of mitochondrial involvement in sarcopenia and define the impact of mitochondria-targeted therapies for the prevention and treatment of sarcopenia.Sarcopenia is defined by the age-related loss of skeletal muscle quality, which relies on mitochondrial homeostasis. During aging, several mitochondrial features such as bioenergetics, dynamics, biogenesis, and selective autophagy (mitophagy) are altered and impinge on protein homeostasis, resulting in loss of muscle mass and function. Thus, mitochondrial dysfunction contributes significantly to the complex pathogenesis of sarcopenia, and mitochondria are indicated as potential targets to prevent and treat this age-related condition. After a concise presentation of the age-related modifications in skeletal muscle quality and mitochondrial homeostasis, the present review summarizes the most relevant findings related to mitochondrial alterations in sarcopenia.
Highlights
The term “sarcopenia” is derived from the combination of two Greek words, sark and penia, and defines the age-related loss of muscle mass and function [1].Changes underlying sarcopenia include both structural and molecular modifications that alter muscle quality and lead to functional impairment
Impaired muscle quality of old age is accompanied by chronic low-grade inflammation, defective anabolic signaling mediated by the growth hormone (GH)/insulin growth factor-1 (IGF-1) pathway, reduced protein intake, and vitamin D
All these findings are linked with the disruption of muscle bioenergetics, which mostly depend on mitochondrial homeostasis and metabolism [8]
Summary
The term “sarcopenia” is derived from the combination of two Greek words, sark (flesh) and penia (loss), and defines the age-related loss of muscle mass and function [1]. Changes underlying sarcopenia include both structural and molecular modifications that alter muscle quality and lead to functional impairment. Impaired muscle quality of old age is accompanied by chronic low-grade inflammation, defective anabolic signaling mediated by the growth hormone (GH)/insulin growth factor-1 (IGF-1) pathway, reduced protein intake, and vitamin D insufficiency [5,6,7]. All these findings are linked with the disruption of muscle bioenergetics, which mostly depend on mitochondrial homeostasis and metabolism [8]. After a brief presentation of age-related mitochondrial modifications in skeletal muscle, the present review presents the latest evidence of the role played by mitochondria in the modulation of muscle metabolism in sarcopenia
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