Figure 8.

Model of membrane repair in human skeletal muscle cells. (A,A’) Entry of Ca²⁺ induces the recruitment of Anx to the plasma membrane, notably AnxA5 and AnxA6. (B,B’) The membrane tension is reduced by depolymerization of actin and exocytosis of lysosomes [42]. The increase in sarcolemma surface leads to excess membrane at the disruption site on which AnxA6 is associated. AnxA5 forms 2D arrays that strengthen the sarcolemma and limit the expansion of the tear, as previously reported [26]. Intracellular vesicles are recruited to the disruption site. (C,C’) Aggregation of intracellular vesicles forms a “patch” that plugs the rupture. AnxA6 and maybe AnxA5, induce the folding of the extensions of sarcolemma in order to form a tight structure. (D,D’) Accumulation of Anx leads to the folding and curvature [28] of membranes and the formation of the cap subdomain. (E,E’) The integrity of the sarcolemma is restored by the newformed plasma membrane and the elimination of the cap subdomain by macrophages (not represented) [43].