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Objective <p>The research focused on examining CpG methylation within the <i>TXNRD2</i> promoter area in chronic heart failure (CHF) patients, aiming to correlate methylation levels with clinical indexes to guide CHF treatment.</p> Methods <p>Whole blood samples from 20 CHF patients and 20 healthy controls were analyzed using MALDI-TOF-MS. Methylation levels of CpGs in the <i>TXNRD2</i>-FA42 region were compared between CHF patients, healthy controls, and CHF patients with varying cardiac functions.</p> Results <p><i>TXNRD2</i>-FA42_CpG_3 methylation was lower in CHF patients (<i>P</i> = 0.0407), while <i>TXNRD2</i>-FA42_CpG_8 was higher (<i>P</i> = 0.0183) compared to controls.</p> Conclusion <p><i>TXNRD2</i> promoter methylation in CHF patients exhibited bidirectional regulation, potentially influencing coagulation, renal function, and blood routine. These results deepen understanding of CHF pathogenesis and suggest new treatment approaches.</p>

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The bidirectional regulatory effect of TXNRD2 methylation in patients with chronic heart failure and its nonlinear dose-response relationship with key clinical parameters

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月4日

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  • Ruonan Zhao,
  • Lin Ma,
  • Ruiping Wang,
  • Rongqiang Zhang

摘要

Objective

The research focused on examining CpG methylation within the TXNRD2 promoter area in chronic heart failure (CHF) patients, aiming to correlate methylation levels with clinical indexes to guide CHF treatment.

Methods

Whole blood samples from 20 CHF patients and 20 healthy controls were analyzed using MALDI-TOF-MS. Methylation levels of CpGs in the TXNRD2-FA42 region were compared between CHF patients, healthy controls, and CHF patients with varying cardiac functions.

Results

TXNRD2-FA42_CpG_3 methylation was lower in CHF patients (P = 0.0407), while TXNRD2-FA42_CpG_8 was higher (P = 0.0183) compared to controls.

Conclusion

TXNRD2 promoter methylation in CHF patients exhibited bidirectional regulation, potentially influencing coagulation, renal function, and blood routine. These results deepen understanding of CHF pathogenesis and suggest new treatment approaches.