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Dysfunctional Wound Healing in Diabetic Foot Ulcers: New Crossroads

  • Microvascular Complications—Neuropathy (R Pop-Busui, Section Editor)
  • Published:
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Abstract

Purpose of Review

Diabetic foot ulcerations (DFU) affect 25% of patients with diabetes mellitus during their lifetime and constitute a major health problem as they are often recalcitrant to healing due to a constellation of both intrinsic and extrinsic factors. The purpose of this review is to (1) detail the current mechanistic understanding of DFU formation and (2) highlight future therapeutic targets.

Recent Findings

From a molecular perspective, DFUs exhibit a chronic inflammatory predisposition. In addition, increased local hypoxic conditions and impaired cellular responses to hypoxia are pathogenic factors that contribute to delayed wound healing. Finally, recent evidence suggests a role for epigenetic alterations, including microRNAs, in delayed DFU healing due to the complex interplay between genes and the environment.

Summary

In this regard, notable progress has been made in the molecular and genetic understanding of DFU formation. However, further studies are needed to translate preclinical investigations into clinical therapies.

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Acknowledgements

We would like to thank Robin Kunkel for her assistance with the scientific illustrations provided in this manuscript.

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  1. Department of Surgery, Section of Vascular Surgery, University of Michigan, 5364 Cardiovascular Center, 1500 E. Medical Center Drive, Ann Arbor, MI, 48109-5867, USA

    Frank M. Davis, Andrew Kimball, Anna Boniakowski & Katherine Gallagher

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  1. Frank M. Davis
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Correspondence to Katherine Gallagher.

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Frank M. Davis, Andrew Kimball, Anna Boniakowski, and Katherine Gallagher declare that they have no conflict of interest.

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This article is part of the Topical Collection on Microvascular Complications—Neuropathy

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Davis, F.M., Kimball, A., Boniakowski, A. et al. Dysfunctional Wound Healing in Diabetic Foot Ulcers: New Crossroads. Curr Diab Rep 18, 2 (2018). https://doi.org/10.1007/s11892-018-0970-z

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