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논문분류	춘계학술대회 초록집
제목	Exploring causal association between circulating inflammatory cytokines and diabetic nephropathy: A bidirectional Mendelian randomization study
저자	Xu Li
출판정보	2024; 2024(1):
키워드
초록	Objectives: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Preclinical research has demonstrated the involvement of inflammation in diabetic nephropathy, yet the causality and the causal direction remain unclear. Methods: Two-sample bidirectional Mendelian randomization (MR) analysis was used in this study. Inflammatory cytokines were obtained from genome-wide association study (GWAS) summary data of 8,293 healthy participants. Summary statistics for DN were sourced from the Finn biobank (n=3,283 cases and 210,463 controls). Inverse variance weighted (IVW) was selected as the primary analysis. MR-Egger, weighted median (WM) were used as complementary methods to examine causality. Additionally, sensitivity analyses including Cochran's Q test, MR-Egger, and leave-one-out analyses were conducted to guarantee the accuracy and robustness of our MR analysis. Results: Suggestive protective effect for DN was identified in interleukin (IL)-10 (OR: 0.87, 95% CI: 0.79-0.97, p = 0.010), while interferon gamma (IFN -γ) was shown to be a risk factor for DN (OR: 1.23, 95% CI: 1.04-1.46, p = 0.013). Furthermore, vascular endothelial growth factor (VEGF), monokine induced by gamma interferon (MIG), monocyte chemoattractant protein-3 (MCP-3), IL-5, IL-9, IL-13, hepatocyte growth factor (HGF) and granulocyte colony stimulating factor (G-CSF) are suggested as upregulated downstream consequences of DN in genetically prediction, while TNF-related apoptosis inducing ligand (TRAIL), platelet-derived growth factor bb (PDGF-bb), interferon-gamma inducible protein of 10 (IP-10) and eotaxin as downregulated consequences. Additionally, genetically predicted bidirectional associations between IL-16 and IL-1 receptor antagonist (IL-1RA) with DN risk were suggested. Result remained robust after applying sensitivity tests. Conclusions: This study suggests a causality between inflammation and DN, exhibiting both upstream and downstream factors of DN. Whether these cytokines can be used to predict or improve DN development requires further researches.
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