Abstract
Skeletal muscle comprises approximately 40% of the total body mass. Preserving muscle health and function is essential for the entire body in order to counteract chronic diseases such as type II diabetes, cardiovascular diseases, and cancer. Prolonged physical inactivity, particularly among the elderly, causes muscle atrophy, a pathological state with adverse outcomes such as poor quality of life, physical disability, and high mortality. In murine skeletal muscle C2C12 cells, increased expression of the spermine oxidase (SMOX) enzyme has been found during cell differentiation. Notably, SMOX overexpression increases muscle fiber size, while SMOX reduction was enough to induce muscle atrophy in multiple murine models. Of note, the SMOX reaction product spermidine appears to be involved in skeletal muscle atrophy/hypertrophy. It is effective in reactivating autophagy, ameliorating the myopathic defects of collagen VI-null mice. Moreover, spermidine treatment, if combined with exercise, can affect D-gal-induced aging-related skeletal muscle atrophy. This review hypothesizes a role for SMOX during skeletal muscle differentiation and outlines its role and that of spermidine in muscle atrophy. The identification of new molecular pathways involved in the maintenance of skeletal muscle health could be beneficial in developing novel therapeutic lead compounds to treat muscle atrophy.
Highlights
Skeletal muscle is the largest tissue of the human body and represents 40–50% of body weight, varying according to physiological and pathological conditions [1]
This review focuses on the role of spermine oxidase (SMOX) in skeletal muscle pathophysiology, underlining its role in myogenesis and muscle atrophy
This review points out that does SMOX take part in cancer and neurological disorders, but it is involved in skeletal muscle pathophysiology
Summary
Skeletal muscle is the largest tissue of the human body and represents 40–50% of body weight, varying according to physiological and pathological conditions [1]. Skeletal muscle atrophy is a frequent and disabling condition. Polyamines (PAs) are essential for normal cell growth, proliferation, and differentiation, and the tissue levels of individual PAs are maintained and buffered via complex regulatory mechanisms [3,4]. PA catabolism is finely regulated by the enzymes N1 -acetyltransferase, polyamine oxidase, and spermine oxidase (SMOX) (Figure 1). The strong association between PA levels and muscle mass is evident, the potential mechanism by which PAs regulate muscle growth is still unclear [10]. This review focuses on the role of SMOX in skeletal muscle pathophysiology, underlining its role in myogenesis and muscle atrophy.
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