Molecular Markers of Endothelial Dysfunction in Post-COVID Prediabetes: A Focus on NOS3 Gene Expression and Pro-Inflammatory Cytokine Profiles

Read the full article See related articles

Listed in

This article is not in any list yet, why not save it to one of your lists.
Log in to save this article

Abstract

Background: Prediabetes, marked by early insulin resistance and chronic low-grade inflammation, is closely linked to endothelial dysfunction and increased cardiovascular risk. Post-COVID-19 recovery may intensify this risk due to persistent vascular inflammation and endothelial damage. This study investigates the relationship between NOS3 gene expression and key pro-inflammatory cytokines (IL-6, IL-18, TNF-α, IL-1β) in post-COVID prediabetic individuals to identify early molecular markers of endothelial malfunction and inform preventive strategies. Methods and Results: A case-control study was conducted with 120 participants (60 post-COVID prediabetics and 60 healthy controls). Blood samples were analyzed for biochemical markers and cytokine levels using ELISA, while NOS3 gene expression was quantified using RT-PCR (normalized to GAPDH via the 2 −ΔΔCt method). Data were analyzed using Stata 17.0. Results indicated significantly elevated levels of IL-6, IL-18, IL-1β, TNF-α, and NOS3 expression in post-COVID prediabetics, suggesting heightened inflammation and endothelial activation. ROC analysis revealed IL-6 and TNF-α as strong discriminatory markers. A positive correlation was observed between NOS3 expression and all cytokines. Logistic regression showed that IL-18, IL-6, and TNF-α were significant independent predictors of NOS3 dysregulation, while IL-1β lost significance after adjustment. Conclusion: This study highlights a clear association between elevated pro-inflammatory cytokines and NOS3 overexpression in post-COVID prediabetes, reflecting a compensatory endothelial response to inflammation. IL-18 emerged as the strongest independent predictor, supporting the potential of NOS3 as an early biomarker for endothelial stress and emphasizing the role of inflammation in cardiometabolic risk post-COVID-19.

Article activity feed