Title:How Does Diabetes Impair Penile Tissues during Erectile Dysfunction?
Volume: 20
Issue: 9
Author(s): Yi-Xing Wu, Chun-Tao Yang, Na Li, Xue Zheng, Xiang Li, Hui Zhang and Jie Shen*
Affiliation:
- Department of Endocrinology and Metabolism, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630,China
Keywords:
Bioinformatics, diabetic erectile dysfunction, penile tissues, insulin resistance, PPI network, protein synthesis.
Abstract:
Background: Erectile dysfunction (ED) is a significant but underestimated complication
during diabetes mellitus (DM). Currently, few special treatments are available clinically due to the lack
of specific therapeutic targets. Genomic analysis can be helpful to find potential targets. In this study,
the gene expression under diabetic ED condition was analyzed using a gene array, and the significance
of the outcomes was evaluated through clinical data.
Methods: The expressions of 15923 genes were analyzed using R software. Differential expression
genes (DEGs) were identified through the constructed volcano plot. The function enrichment of Gene
Ontology (GO) and KEGG was screened with the DAVID online tool. The interaction between these
DEGs was revealed through constructing a protein-protein interaction network and the hub genes were
uncovered using the STRING and Cytoscape tool. Lastly, the data of diabetic ED patients were applied
to verify the bioinformatics findings.
Results: The study showed that 75 genes in the rat penile tissues were upregulated, while 97 genes
were downregulated on the diabetic ED condition. These genes were mainly involved in extracellular
matrix composition, collagen fibril organization, as well as protein digestion & absorption. Additionally,
insulin-related signaling pathways were affected. The clinical analysis indicated that insulin resistance
was associated with the diabetic ED severity. Notably, the bioinformatics analysis also suggested
that ferroptosis pathway was probably activated under the diabetic ED condition.
Conclusion: The impaired protein synthesis induced by deficient insulin signaling is an important
cause of the diabetic ED. The improvement of protein synthesis through restoring insulin function may
be potentially useful for diabetic ED therapy.
