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Copyright ©The Author(s) 2021.
World J Clin Cases. May 16, 2021; 9(14): 3227-3237
Published online May 16, 2021. doi: 10.12998/wjcc.v9.i14.3227
Figure 1
Figure 1 Putative mechanism of physiotherapy on the dying skin flap as induction of angiogenesis through inhibiting sympathetic nerve for vasodilation and promoting the secretion of vascular endothelial growth factor secretion. Akt/PKB: Protein kinase B; Erk: Extracellular signal-regulated kinase; MEK: Mitogen-activated protein kinase kinase; Pl3K: Phosphatidylinositol 3-kinase; VEGF: Vascular endothelial growth factor; VEGFR: Vascular endothelial growth factor receptor; Raf: Rapidly accelerated fibrosarcoma.
Figure 2
Figure 2 Putative molecular mechanism of physiotherapeutic methods for upregulation of heat shock protein 32 and heat shock protein 70 in the skin flap, which promotes vasodilation and inhibition of apoptosis. Apaf-1: Apoptosis protease-activating factor-1; HSP: Heat shock protein; JNK: Jun N-terminal kinase; p38: Protein 38.