• Nicole C Nowak, Daniela M Menichella, Richard Miller, and Amy S Paller.
• Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
• Transl Res. 2021 Oct 1; 236: 87-108.

AbstractType 2 diabetes is associated with several potential comorbidities, among them impaired wound healing, chronic ulcerations, and the requirement for lower extremity amputation. Disease-associated abnormal cellular responses, infection, immunological and microvascular dysfunction, and peripheral neuropathy are implicated in the pathogenesis of the wound healing impairment and the diabetic foot ulcer. The skin houses a dense network of sensory nerve afferents and nerve-derived modulators, which communicate with epidermal keratinocytes and dermal fibroblasts bidirectionally to effect normal wound healing after trauma. However, the mechanisms through which cutaneous innervation modulates wound healing are poorly understood, especially in humans. Better understanding of these mechanisms may provide the basis for targeted treatments for chronic diabetic wounds. This review provides an overview of wound healing pathophysiology with a focus on neural involvement in normal and diabetic wound healing, as well as future therapeutic perspectives to address the unmet needs of diabetic patients with chronic wounds.Copyright © 2021 Elsevier Inc. All rights reserved.

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