ArticleAmerican journal of translational research2025
Altered expression of miR-132, miR-155, VEGF, and IGF-1 as key indicators in the pathogenesis of diabetic foot infection.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimsThis study aimed to investigate the alterations of miR-132, miR-155, vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1) expression in patients with diabetic foot infection (DFI), and to analyze and the distribution of pathogenic microorganisms, with the goal of elucidating underlying molecular mechanisms and identifying potential diagnostic and therapeutic biomarkers.
methodsA retrospective analysis was conducted on 114 patients with diabetic foot, who were divided into two groups: an observation group (n = 56) comprising patients with DFI, and a control group (n = 58) without infection. The primary outcomes included the expression levels of miR-132, miR-155, VEGF, and IGF-1, as well as microbial profiles isolated from infected wound sites. Secondary outcomes encompassed inflammatory markers [C-reactive protein (CRP), white blood cell count (WBC), interleukin-6 (IL-6), procalcitonin (PCT)], biochemical markers [fasting glucose, glycated hemoglobin (HbA1c), lipid profile], and hormonal markers [cortisol, thyroid-stimulating hormone (TSH), growth hormone (GH), and leptin].
resultsMicrobiological cultures identified Staphylococcus aureus, Pseudomonas aeruginosa, and Escherichia coli as the predominant pathogens in DFI cases, with a mixed infection observed in a subset. Expression levels of miR-132 (5.6 ± 1.2 vs. 2.3 ± 0.5, P < 0.001), miR-155 (4.8 ± 1.1 vs. 1.9 ± 0.6, P < 0.001), VEGF (245.3 ± 32.5 pg/mL vs. 150.7 ± 25.3 pg/mL, P < 0.001), and IGF-1 (182.4 ± 30.6 pg/mL vs. 124.8 ± 21.7 pg/mL, P < 0.001) were significantly upregulated in the observation group compared to controls, suggesting their involvement in the pathogenesis of DFI. Inflammatory and biochemical markers were markedly elevated in the observation group (P < 0.001), reflecting systemic inflammation and metabolic dysregulation. Hormonal analysis revealed increased cortisol and insulin levels, along with decreased TSH, GH, and leptin levels (P < 0.001). Additionally, significant negative correlations were found between miR-132/miR-155 and VEGF/IGF-1, indicating potential regulatory interactions in the context of inflammation and vascular remodeling (P < 0.001).
conclusionElevated expression of miR-132, miR-155, VEGF, and IGF-1, together with characteristic microbial profiles, plays a critical role in the pathogenesis of DFI. These molecules may serve as promising biomarkers for disease diagnosis and therapeutic monitoring.
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