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Background <p>Diabetic nephropathy (DN) and diabetic cardiomyopathy (DCM) are major complications of type 2 diabetes mellitus (T2DM), but the contribution of immune-inflammatory mechanisms to their pathogenesis remains incompletely understood. This exploratory study investigated circulating inflammatory factors potentially associated with DN and subclinical left ventricular systolic dysfunction (LVSD) in T2DM.</p> Methods <p>Twenty patients with T2DM were enrolled and stratified by DN status (n = 14) and GLS-defined subclinical LVSD (absolute GLS &lt; 18%; n = 12). Serum levels of 48 cytokines were measured using a multiplex immunoassay. Group differences in inflammatory factors were compared, and exploratory protein–protein interaction (PPI) network analysis was performed on nominally differential factors.</p> Results <p>Four cytokines—M-CSF, SCF, IL-16, and IL-17—showed nominally higher levels in the DN group than in the T2DM without nephropathy group, whereas SCF and MIP-1α showed nominal elevation in the GLS-defined subgroup analysis. Systemic inflammatory indices, including the neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory response index (SIRI), were also higher in DN. However, after Benjamini–Hochberg false discovery rate correction for multiple comparisons, none of the observed cytokine differences remained statistically significant. Exploratory ROC analyses suggested apparent within-sample discriminatory performance, but these estimates should be interpreted cautiously because candidate marker selection and performance evaluation were conducted in the same small dataset. SCF was the only inflammatory marker showing nominal associations in both the renal and GLS-based analyses in this cohort.</p> Conclusion <p>This small exploratory study observed several nominal inflammatory signals associated with DN and subclinical LVSD in T2DM; however, none of the cytokine associations remained statistically significant after multiple-comparison correction. These findings should therefore be regarded as hypothesis-generating only. Among the observed signals, SCF showed nominal associations with both renal involvement and early subclinical myocardial dysfunction and may warrant further evaluation in larger, independent studies.</p>

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Exploratory analysis of circulating inflammatory factors associated with diabetic nephropathy and subclinical systolic dysfunction in type 2 diabetes mellitus

  • 期刊论文

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  • 发表日期：

    2026年5月4日

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  • Xiaoxu Yang,
  • Yinjia Zhang,
  • Qing Lv,
  • Yao Liu,
  • Cuiping Jiang,
  • Xiaoli Zhang

摘要

Background

Diabetic nephropathy (DN) and diabetic cardiomyopathy (DCM) are major complications of type 2 diabetes mellitus (T2DM), but the contribution of immune-inflammatory mechanisms to their pathogenesis remains incompletely understood. This exploratory study investigated circulating inflammatory factors potentially associated with DN and subclinical left ventricular systolic dysfunction (LVSD) in T2DM.

Methods

Twenty patients with T2DM were enrolled and stratified by DN status (n = 14) and GLS-defined subclinical LVSD (absolute GLS < 18%; n = 12). Serum levels of 48 cytokines were measured using a multiplex immunoassay. Group differences in inflammatory factors were compared, and exploratory protein–protein interaction (PPI) network analysis was performed on nominally differential factors.

Results

Four cytokines—M-CSF, SCF, IL-16, and IL-17—showed nominally higher levels in the DN group than in the T2DM without nephropathy group, whereas SCF and MIP-1α showed nominal elevation in the GLS-defined subgroup analysis. Systemic inflammatory indices, including the neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory response index (SIRI), were also higher in DN. However, after Benjamini–Hochberg false discovery rate correction for multiple comparisons, none of the observed cytokine differences remained statistically significant. Exploratory ROC analyses suggested apparent within-sample discriminatory performance, but these estimates should be interpreted cautiously because candidate marker selection and performance evaluation were conducted in the same small dataset. SCF was the only inflammatory marker showing nominal associations in both the renal and GLS-based analyses in this cohort.

Conclusion

This small exploratory study observed several nominal inflammatory signals associated with DN and subclinical LVSD in T2DM; however, none of the cytokine associations remained statistically significant after multiple-comparison correction. These findings should therefore be regarded as hypothesis-generating only. Among the observed signals, SCF showed nominal associations with both renal involvement and early subclinical myocardial dysfunction and may warrant further evaluation in larger, independent studies.