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Background <p>End-stage renal disease (ESRD) is frequently accompanied by major adverse cardiac and cerebrovascular events (MACCE) in affected patients. Therefore, there is an urgent need to develop effective biomarkers.</p> Methods <p>This prospective study included 112 ESRD patients (62 with MACCE, 50 Non-MACCE), with baseline clinical data and blood samples collected for all subjects. We quantified miR-223 expression through RT-qPCR. To clarify the independent predictive value of miR-223, we conducted multivariate logistic analysis to verify its independent association with the occurrence of MACCE, and drew ROC curves to evaluate its ability to distinguish the occurrence or non-MACCE. Then, we induced inflammation in HUVECs with TNF-α, transfected miR-223 overexpression vectors into these cells, and observed corresponding changes in inflammatory cytokines, adhesion molecules, endothelial markers, nitric oxide metabolites, and cell proliferation.</p> Results <p>Clinical analysis of ESRD patients revealed that the development of MACCE was associated with significantly lower baseline expression of miR-223 compared to the non-MACCE group. Multivariate analysis confirmed low levels of miR-223 as an independent predictor of MACCE with robust discriminatory ability (AUC = 0.896). In addition, miR-223 levels were inversely related to inflammatory markers (hs-CRP) and serum phosphorus and iPTH. In vitro, miR-223 overexpression suppressed inflammation, the expression of adhesion molecules, ET-1 secretion, normalized nitrite levels, and inhibited aberrant endothelial proliferation.</p> Conclusion <p>This study confirms that reduced miR-223 is an independent predictor of MACCE risk in ESRD patients, with confirmed multifaceted endothelial protective effects in vitro. miR-223 could be a new biomarker integrating multiple risk pathways for cardiovascular risk assessment.</p>

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Low miR-223 links to major adverse cardiovascular and cerebrovascular events in end-stage renal disease through endothelial damage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月16日

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  • Jie Liao,
  • Xueling Cao,
  • Lili Yu

摘要

Background

End-stage renal disease (ESRD) is frequently accompanied by major adverse cardiac and cerebrovascular events (MACCE) in affected patients. Therefore, there is an urgent need to develop effective biomarkers.

Methods

This prospective study included 112 ESRD patients (62 with MACCE, 50 Non-MACCE), with baseline clinical data and blood samples collected for all subjects. We quantified miR-223 expression through RT-qPCR. To clarify the independent predictive value of miR-223, we conducted multivariate logistic analysis to verify its independent association with the occurrence of MACCE, and drew ROC curves to evaluate its ability to distinguish the occurrence or non-MACCE. Then, we induced inflammation in HUVECs with TNF-α, transfected miR-223 overexpression vectors into these cells, and observed corresponding changes in inflammatory cytokines, adhesion molecules, endothelial markers, nitric oxide metabolites, and cell proliferation.

Results

Clinical analysis of ESRD patients revealed that the development of MACCE was associated with significantly lower baseline expression of miR-223 compared to the non-MACCE group. Multivariate analysis confirmed low levels of miR-223 as an independent predictor of MACCE with robust discriminatory ability (AUC = 0.896). In addition, miR-223 levels were inversely related to inflammatory markers (hs-CRP) and serum phosphorus and iPTH. In vitro, miR-223 overexpression suppressed inflammation, the expression of adhesion molecules, ET-1 secretion, normalized nitrite levels, and inhibited aberrant endothelial proliferation.

Conclusion

This study confirms that reduced miR-223 is an independent predictor of MACCE risk in ESRD patients, with confirmed multifaceted endothelial protective effects in vitro. miR-223 could be a new biomarker integrating multiple risk pathways for cardiovascular risk assessment.