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Dermatology Journal

ISSN: 2769-240X

Short Communication Open Access
Volume 1 | Issue 1 | DOI: https://doi.org/10.46439/derma.1.004

Upregulation of long noncoding RNA growth arrest-specific 5 mediates pro-inflammatory mechanisms of diabetic wound healing impairment

Shaquia Idlett-Ali1, Kenneth Liechty1, Junwang Xu2.*
  • 1Laboratory for Fetal and Regenerative Biology, Department of Surgery, University of Colorado, Denver-Anschutz Medical Campus and Children’s Hospital of Colorado, Aurora, Colorado 80045, USA
  • 2Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA
+ Affiliations - Affiliations

Corresponding Author

Junwang Xu, jxu61@uthsc.edu

Received Date: March 24, 2021

Accepted Date: June 23, 2021

Citation:

Idlett-Ali S, Liechty K, Xu J. Upregulation of long noncoding RNA growth arrest-specific 5 mediates pro-inflammatory mechanisms of diabetic wound healing impairment. Dermatol J. 2021; 1(1):8-10.


Copyright: © 2021 Idlett-Ali S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Unresolved inflammatory processes contribute to impaired healing in diabetic wounds, with increasing evidence implicating persistent pro-inflammatory macrophage polarization as a driver of chronic inflammation and delayed wound closure. Previous investigations aimed to uncover the role of regulatory RNAs in macrophage polarization and to understand how aberrant expression patterns contribute to wound healing impairment, with the goal of identifying novel therapeutic targets for promoting normal wound healing progression. In the Journal of Investigative Dermatology, Hu et al. reveal a role of the tumor suppressor, long noncoding RNA (lncRNA) Growth Arrest-Specific 5 (GAS5), in regulating macrophage polarization. Of note, their findings suggest that hyperglycemia induces overexpression of GAS5 which subsequently results in a greater production of the pro-inflammatory macrophage phenotype. Knockdown of GAS5 in diabetic wounds normalized healing time, highlighting the potential therapeutic value of targeting GAS5 for enhanced wound healing progression.

Keywords

Diabetes, lncRNA GAS5, Wound healing, Macrophage polarization

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Upregulation of long noncoding RNA growth arrest-specific 5 mediates pro-inflammatory mechanisms of diabetic wound healing impairment

Unresolved inflammatory processes contribute to impaired healing in diabetic wounds, with increasing evidence implicating persistent pro-inflammatory macrophage polarization as a driver of chronic inflammation and delayed wound closure. Previous investigations aimed to uncover the role of regulatory RNAs in macrophage polarization and to understand how aberrant expression patterns contribute to wound healing impairment, with the goal of identifying novel therapeutic targets for promoting normal wound healing progression. In the Journal of Investigative Dermatology, Hu et al. reveal a role of the tumor suppressor, long noncoding RNA (lncRNA) Growth Arrest-Specific 5 (GAS5), in regulating macrophage polarization.

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