Mechanistic analysis of abnormal key enzymes in the arginine and proline metabolic pathways in diabetic bone injury

Objective: Based on the GSE189112 dataset, this study aimed to systematically analyze the abnormal expression patterns of the arginine and proline metabolic pathways in a streptozotocin (STZ)-induced diabetic model, clarify the regulatory mechanism of abnormal key enzymes in this pathway on diabetic bone injury, and provide a theoretical basis for the development of metabolic regulatory targets for diabetic bone injury. Methods: The GSE189112 dataset from the Gene Expression Omnibus (GEO) database was used as the analysis object. The limma package in R/Bioconductor software was employed to screen for differentially expressed genes (DEGs) with thresholds of |log₂FoldChange| > 0.5 and P < 0.05. The clusterProfiler package was used to perform enrichment analysis on the screened DEGs. Results: Quality control of the data showed that the sample expression profiles in the GSE189112 dataset exhibited a consistent distribution with good reliability. DEGs were significantly enriched in biological processes such as "cytoplasmic translation". Key enzymes in the arginine and proline metabolic pathways showed significant differential expression: arginine decarboxylase (ADC) and creatine kinase were upregulated, while nitric oxide synthase (NOS), 1-pyrroline-5-carboxylate dehydrogenase (P5CDH), proline dehydrogenase (PRODH), S-adenosylmethionine decarboxylase, and aspartate transaminase (GOT) were downregulated. Conclusion: Dysregulation of the arginine and proline metabolic pathways is one of the core mechanisms of bone injury in diabetic mice. The differentially expressed key enzymes in this pathway can serve as potential metabolic regulatory targets for diabetic bone injury, providing theoretical support for subsequent screening of active molecule modification strategies and design of bone repair biomaterials.

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