ArticleDermatology journal2021
Upregulation of long noncoding RNA growth arrest-specific 5 mediates pro-inflammatory mechanisms of diabetic wound healing impairment.
Article in Dermatology journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 0 citations in OpenAlex.
- The role and mechanism by which micropeptide WHPP promote refractory wound healing.Journal of translational medicine · 2026Article
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3 authors at 1 institution in 1 country.
Funding
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.
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