AI Article Synopsis
- Maternal hyperhomocysteinemia is known to independently increase the risk of congenital heart disease (CHD), but the impact of high paternal homocysteine levels on CHD is not well understood.!*
- In a study with male mice, high homocysteine levels led to reduced sperm quality and increased ventricular septal defects (VSD) in their offspring, linked to changes in sperm DNA methylation.!*
- Folic acid supplementation was shown to reduce the incidence of VSD in offspring from high homocysteine male mice, suggesting that lowering paternal homocysteine could be a potential strategy to prevent CHD in children.!*
Article Abstract
Maternal hyperhomocysteinemia is widely considered as an independent risk of congenital heart disease (CHD). However, whether high paternal homocysteine causes CHD remains unknown. Here, we showed that increased homocysteine levels of male mice caused decreased sperm count, sperm motility defect and ventricular septal defect of the offspring. Moreover, high levels of paternal homocysteine decrease sperm DNMT3A/3B, accompanied with changes in DNA methylation levels in the promoter regions of CHD-related genes. Folic acid supplement could decrease the occurrence of VSD in high homocysteine male mice. This study reveals that increased paternal homocysteine level increases VSD risk in the offspring, indicating that decreasing paternal homocysteine may be an intervening target of CHD.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10960133 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.109447 | DOI Listing |
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