**1. Introduction**

Skeletal muscle growth and regeneration is dependent on the activation of mitotically quiescent resident cells known as skeletal muscle satellite cells (SC) located beneath the basal lamina (integral part of basement membrane) on the plasma membrane (sarcolemma) of adult skeletal muscle fibers. Activated by muscle injury including work overload (i.e., weight lifting), satellite cells proliferate making myogenic precursor cells (myoblasts) that migrate to the site of injury and after withdrawal from the cell cycle fuse collectively or with damaged fibers. The fusion process is mediated by plasma membrane proteins, some of which are the receptors for intermediate of lipid metabolism such as sphingosine 1-phosphate (sphingolipid, S1P). A great deal of plasma membrane surface and integral proteins at the extracellular site is glycosylated and prenylated, the processes indispensable for intracellular protein transport (from endo‐ plasmic reticulum to Golgi apparatus, and from trans-Golgi network to the plasma membrane) as well as for lateral and vertical protein translocation within sarcolemma. In adult skeletal muscle, the self-renewing capacity of satellite cells contributes to muscle growth, and regen‐ eration-associated hypertrophy as skeletal muscle-specific adaptation to workload. Hypertro‐ phy also occurs in satellite cell-depleted skeletal muscle, although in this case neither increase in myonuclei in satellite cell-depleted fibers nor the muscle regenerates after BaCl2-induced severe muscle damage [1]. Accordingly, the biochemistry and structural modifications of plasma membrane are seemingly indispensable for the commitment of satellite cells and their progeny of myoblasts to skeletal muscle renewal. In this review, we hypothesized that changes in the sarcolemmal composition of proteome, glycoproteome, and/or lipidome are the major determinants of satellite cells and muscle fibers to regenerate skeletal muscle. From the experiments and clinical observations related to statin-induced myopathy [2–4] as well as the successful efforts aiming to correct plasma membrane integrity by the modification of skeletal muscle plasma membrane fluidity, we conclude that closer examination of the plasma membrane composition and structural organization might shed more light on the molecular mechanisms of satellite cell commitment to muscle rejuvenation.
