Investigates how oxidative stress from ischemia/reperfusion causes actin filament depolymerization and membrane damage in skeletal muscle cells, with poloxamer 188 (a membrane sealing agent) as a protective intervention. Thymosin β4, as the G-actin/F-actin equilibrium regulator, provides mechanistic context for why actin depolymerization under oxidative stress is pathological—the disruption of the normal TB4-regulated actin equilibrium contributes to pressure ulcer and reperfusion injury damage. While focused on poloxamer rather than TB4, documents the critical role of actin regulation in oxidative muscle injury.
Wong, Sing Wan; Yao, Yifei; Hong, Ye; Ma, Zhiyao; Kok, Stanton H L; Sun, Shan; Cho, Michael; Lee, Kenneth K H; Mak, Arthur F T