Soft tissue damage stimulates sympathetic nerves to release large amounts of catecholamine hormones which bind to β-adrenergic receptors (β-ARs) on the cell membrane surface. It activates the downstream effector molecules and impairs soft tissue wound healing. β-blockers specifically inhibit β-ARs activation in acute/chronic skin lesions and ulcerative hemangiomas. They also accelerate soft tissue wound healing by shortening the duration of inflammation, speeding keratinocyte migration and reepithelialization, promoting wound contraction and angiogenesis, and inhibiting bacterial virulence effects. In addition, β-blockers shorten wound healing periods in patients with severe thermal damage by reducing the hypermetabolic response. While β-blockers promote/inhibit corneal epithelial cell regeneration and restores limbal stem/progenitor cells function, it could well accelerate/delay corneal wound healing. Given these meaningful effects, a growing number of studies are focused on examining the efficacy and safety of β-blockers in soft tissue wound repair, including acute and chronic wounds, severe thermal damage, ulcerated infantile hemangioma, corneal wounds, and other soft tissue disorders. However, an intensive investigation on their acting mechanisms is imperatively needed. The purpose of this article is to summerize the roles of β-blockers in soft tissue wound healing and explore their clinical applications.
Keywords: keratinocyte migration; mechanism; wound healing; β-adrenoceptor blocker.
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