Cutaneous innervation in impaired diabetic wound healing

Nicole C. Nowak, Daniela M. Menichella, Richard Miller, Amy S. Paller*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

78 Scopus citations

Abstract

Type 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.

Original languageEnglish (US)
Pages (from-to)87-108
Number of pages22
JournalTranslational Research
Volume236
DOIs
StatePublished - Oct 2021

Funding

Drs Paller, Menichella, and Miller acknowledge salary support from NIAMS/NIH grant R01AR077691 for research related to sensory innervation in diabetic wounds.

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Physiology (medical)
  • Biochemistry, medical

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