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A study on the methylation patterns of DIO3 in patients with heart failure and its correlation with key clinical
Qi Miao1, Min Zhang1, Aoyue He2
1Affiliated Hospital, Shaanxi University of Chinese Medicine, Shaanxi, Xianyang, 712000, PR China.
Insights
Heart failure (HF) patients show reduced DNA methylation in DIO3-FA26 promoter regions. These methylation changes correlate with disease severity and clinical markers, suggesting new therapeutic targets for HF.
Area of Science:
- Cardiovascular Biology
- Epigenetics
- Molecular Medicine
Background:
- Heart failure (HF) is a complex syndrome with multifactorial etiology.
- Epigenetic modifications, such as DNA methylation, are increasingly recognized as critical regulators in cardiovascular disease.
- The role of specific gene promoter methylation in HF pathophysiology remains incompletely understood.
Purpose of the Study:
- To investigate the DNA methylation patterns of CpG sites within the DIO3-FA26 promoter region in patients with heart failure.
- To explore the association between differential CpG methylation levels in DIO3-FA26 and clinical parameters in HF patients.
Main Methods:
- Peripheral blood samples were collected from 20 HF patients and 20 healthy controls.
- Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was employed to analyze CpG methylation in the DIO3-FA26 promoter.
- Methylation levels were compared between HF patients and controls, and across different cardiac function classifications within HF.
Main Results:
- A significant decrease in DIO3-FA26_CpG_17.18 methylation was observed in HF patients compared to healthy individuals (P=0.0002).
- Patients with advanced HF (NYHA class III/IV) exhibited significantly lower methylation levels of DIO3-FA26_CpG_24.25.26.27 compared to those with milder HF (NYHA class I/II) (P=0.0168).
- DIO3-FA26 methylation variations were correlated with alterations in coagulation, liver function, kidney function, and routine blood indices (e.g., D-dimer, albumin, calcium, hemoglobin).
Conclusions:
- Reduced methylation of DIO3-FA26_CpG_17.18 is a hallmark of heart failure.
- Decreased methylation of DIO3-FA26_CpG_24.25.26.27 is associated with more severe cardiac dysfunction.
- Epigenetic regulation of DIO3-FA26 by DNA methylation plays a role in HF development and progression, offering potential novel therapeutic targets.
Objective:
This study aimed to analyze the methylation pattern of deoxyribonucleic acid (CpG) sites in the DIO3_FA26 promoter region of patients with heart failure (HF) and explore the correlation between differential CpG methylation levels and various clinical parameters.
Methods:
Peripheral blood specimens were collected from 20 patients with HF and 20 healthy individuals. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry was used to identify and detect the CpG sites in the DIO3_FA26 promoter region. CpG methylation levels were compared between patients with HF and healthy controls and patients with HF with different levels of cardiac function.
Results:
The methylation level of DIO3_FA26_CpG_17.18 in patients with HF was significantly lower than that in the healthy control group (P = 0.0002). Among patients with HF and cardiac function levels of I/II and III/IV, methylation levels of DIO3_FA26_CpG_24.25.26.27 (P = 0.0168) were significantly lower in those with III/IV cardiac function compared to those with I/II cardiac function.
Conclusion:
The methylation level of DIO3_FA26_CpG_17.18 is significantly reduced in patients with HF, and that of DIO3_FA26_CpG_24.25.26.27 is significantly decreased in patients with III/IV cardiac function. Variations in DIO3_FA26 methylation levels influence coagulation, liver and kidney functions, and routine blood indexes, including D-dimer, albumin, calcium, and hemoglobin. This study provides clinical evidence for the involvement of DIO3_FA26 methylation in the occurrence and development of HF and proposes novel targets for HF prevention and treatment.
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