Upregulation of circ_0080968 in diabetic foot ulcer inhibits wound healing via repressing the migration and promoting proliferation of keratinocytes

Fu, Zhonghua; Jiang, Zhengying; Liao, Xincheng; Liu, Mingzhuo; Guo, Guang-hua; Wang, X; Yang, Guangping; Zhou, Zhiyu; Long, Hu; Xiong, Zhenfang

doi:10.1016/j.gene.2023.147669

Cited by 1 publication

(1 citation statement)

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“…Both DFU and psoriasis are related to abnormal keratinocyte functionality (Granata et al, 2019). DFU patients exhibit slow re-epithelialization of keratinocytes along with a chronic inflammatory environment and healing disorders at lesion sites (Yang et al, 2022;Fu et al, 2023). Previous studies showed that the S100A7 mouse model of psoriasis exhibited lesions that were characterized by leukocyte inflammation (Webb et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Identification of a shared gene signature and biological mechanism between diabetic foot ulcers and cutaneous lupus erythemnatosus by transcriptomic analysis

Wu,

Wang,

Duan

et al. 2024

Front. Physiol.

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Diabetic foot ulcers (DFU) and cutaneous lupus erythematosus (CLE) are both diseases that can seriously affect a patient’s quality of life and generate economic pressure in society. Symptomatically, both DLU and CLE exhibit delayed healing and excessive inflammation; however, there is little evidence to support a molecular and cellular connection between these two diseases. In this study, we investigated potential common characteristics between DFU and CLE at the molecular level to provide new insights into skin diseases and regeneration, and identify potential targets for the development of new therapies. The gene expression profiles of DFU and CLE were obtained from the Gene Expression Omnibus (GEO) database and used for analysis. A total of 41 common differentially expressed genes (DEGs), 16 upregulated genes and 25 downregulated genes, were identified between DFU and CLE. GO and KEGG analysis showed that abnormalities in epidermal cells and the activation of inflammatory factors were both involved in the occurrence and development of DFU and CLE. Protein-protein interaction network (PPI) and sub-module analysis identified enrichment in seven common key genes which is KRT16, S100A7, KRT77, OASL, S100A9, EPGN and SAMD9. Based on these seven key genes, we further identified five miRNAs(has-mir-532-5p, has-mir-324-3p,has-mir-106a-5p,has-mir-20a-5p,has-mir-93-5p) and7 transcription factors including CEBPA, CEBPB, GLI1, EP30D, JUN,SP1, NFE2L2 as potential upstream molecules. Functional immune infiltration assays showed that these genes were related to immune cells. The CIBERSORT algorithm and Pearson method were used to determine the correlations between key genes and immune cells, and reverse key gene-immune cell correlations were found between DFU and CLE. Finally, the DGIbd database demonstrated that Paquinimod and Tasquinimod could be used to target S100A9 and Ribavirin could be used to target OASL. Our findings highlight common gene expression characteristics and signaling pathways between DFU and CLE, indicating a close association between these two diseases. This provides guidance for the development of targeted therapies and mutual interactions.

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Section: Discussionmentioning

confidence: 99%