Related Experiment Video
Updated: Jun 29, 2025
In utero Measurement of Heart Rate in Mouse by Noninvasive M-mode Echocardiography
Published on: November 22, 2013
High paternal homocysteine causes ventricular septal defects in mouse offspring
Lian Liu1, Xuan Zhang1, Hao-Ran Geng2,3
1Children's Hospital of Fudan University and Shanghai Genitourinary Cancer Institute Fudan University, Department of Urology, Fudan University Shanghai Cancer Center, Shanghai 201102, China.
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.
