Abstract
Skeletal muscle atrophy or wasting accompanies various chronic illnesses and the aging process, thereby reducing muscle function. One of the most important components contributing to effective muscle repair in postnatal organisms, the satellite cells (SCs), have recently become the focus of several studies examining factors participating in the atrophic process. We critically examine here the experimental evidence linking SC function with muscle loss in connection with various diseases as well as aging, and in the subsequent recovery process. Several recent reports have investigated the changes in SCs in terms of their differentiation and proliferative capacity in response to various atrophic stimuli. In this regard, we review the molecular changes within SCs that contribute to their dysfunctional status in atrophy, with the intention of shedding light on novel potential pharmacological targets to counteract the loss of muscle mass.
Highlights
Skeletal muscle atrophy is characterized by a loss of muscle mass and force, that occurs in response to a variety of pathological and physiological stimuli such as aging, cancer, chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF), diabetes, AIDS infection, sepsis, burns, muscle disuse, loss of muscle innervation, malnutrition, steroidinduced catabolic stimulation, and different congenital neuromuscular diseases (Bonaldo and Sandri, 2013; Egerman and Glass, 2014; Cohen et al, 2015)
It is becoming increasingly evident that understanding the basic molecular mechanisms underlying various forms of atrophy is crucial to develop defined parameters and describe distinct features that categorize different forms of atrophy
It is possible that different forms of atrophy could co-exist, such as disuse atrophy that accompanies aging coupled to bedridden conditions, as a result of chronic debilitating illnesses
Summary
Skeletal muscle atrophy is characterized by a loss of muscle mass and force, that occurs in response to a variety of pathological and physiological stimuli such as aging, cancer, chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF), diabetes, AIDS infection, sepsis, burns, muscle disuse, loss of muscle innervation, malnutrition, steroidinduced catabolic stimulation, and different congenital neuromuscular diseases (Bonaldo and Sandri, 2013; Egerman and Glass, 2014; Cohen et al, 2015). We focus on studies reporting functional changes in SCs resulting from alterations in these pathways, which possibly contribute to the loss of muscle mass.
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