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Inflammation,proliferation and tissue remodeling are essential processes for wound healing.The critical steps are jump-starting and skin cell migration.In the cutaneous wound,the edge of the wound suffers from vascular disruption and high oxygen consumption,and the environment of the wound become hypoxic.Thus promote cell migration by hypoxia-hsp90α-LRP-1 autocrine loop.To identify the burn woundhealing target,We investigate the expression property of hsp90-αaround the edge of the burn wound and found a transient rising in mRNA and protein levels.Also the heat shock skin cell-HACAT,confirrmed these consequences.17-dimethyl aminoet-hylamino-17demethoxygeldanamycin hydrochloride (17-DMAG),an inhibitor of hsp90α,allowed us to identify it as a factor used for comparise the function of hsp90α.It induced heat shock cell cycle arrest,apoptosis and inhibit migration.Finally,topical application of hsp90αthe first five days on the second bum wound significantly reduced the size of the wound healing at every observed time points,inflammation was slightly and granulation tissue was developed,also the epidermal cells at the wound margins progressed more rapidly with no adverse effect on the healing process.We demonstrated overexpression of hsp90αin the early phases of wound healing can improve burn wound healing.Thus need to consider hsp90αin future wound healing therapies.