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LncRNA 91234.1 targets PRMT1/ASCL4/GPX4 axis to regulate formaldehyde-induced cardiomyocyte ferroptosis and
Sijia Zhao1, Pin Sun1, Chao Wang2
1Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao 266000, PR China.
Insights
Formaldehyde exposure causes congenital heart disease (CHD) by promoting ferroptosis through lncRNA 91,234.1 (lnc91234). This study identifies lnc91234 as a potential therapeutic target for treating cardiac dysplasia and CHD.
Area of Science:
- Cardiovascular Biology
- Environmental Toxicology
- Molecular Genetics
Background:
- Congenital heart disease (CHD) is a leading cause of neonatal mortality and a prevalent congenital malformation.
- Both genetic and environmental factors contribute to CHD development, with formaldehyde (FA) emerging as a significant environmental toxin.
- Long noncoding RNAs (lncRNAs) are implicated in cardiac development, and their dysregulation may link FA exposure to cardiac impairments.
Purpose of the Study:
- To elucidate the role of lncRNA in the pathological mechanisms of formaldehyde-induced congenital heart disease (CHD).
- To investigate the specific lncRNA, lncRNA 91,234.1 (lnc91234), and its involvement in FA-induced cardiac dysfunction.
- To identify potential therapeutic targets for cardiac dysplasia and CHD related to FA exposure.
Main Methods:
- Subjecting H9C2 cells to 24-hour formaldehyde exposure.
- Administering formaldehyde (2.0 mg/kg) to female rats and examining their offspring.
- Analyzing the PRMT1/ASCL4/GPX4 axis, H4R3 methylation, lipid peroxidation, and malondialdehyde (MDA) accumulation.
Main Results:
- Formaldehyde exposure induces congenital heart disease (CHD) in offspring.
- lncRNA 91,234.1 (lnc91234) facilitates ferroptosis via the PRMT1/ASCL4/GPX4 axis in formaldehyde-induced cardiac damage.
- This mechanism involves H4R3 methylation, leading to lipid peroxidation and malondialdehyde (MDA) accumulation.
Conclusions:
- Formaldehyde exposure disrupts cardiac function through ferroptosis, a novel finding in CHD pathogenesis.
- lnc91234 is identified as a key mediator in formaldehyde-induced cardiac dysplasia.
- lnc91234 represents a potential therapeutic target for modulating myocardial function in cardiac dysplasia and CHD.
Abstract:
Congenital heart disease (CHD) are the predominant cause of neonatal mortality and the most prevalent congenital malformation. Additionally, CHD can impact cardiovascular health in adulthood and exacerbate cardiovascular conditions in the elderly. Emerging studies indicate that both genetic predispositions and environmental factors may contribute to the development of this condition. Notably, formaldehyde (FA), a ubiquitous environmental toxin, has been increasingly implicated in the pathophysiology of CHD through recent investigations. Earlier, we identified long noncoding RNAs (lncRNAs) that exhibited significant differential expression in rats with cardiac developmental impairments associated with FA exposure. Here our study aims to elucidate the role of lncRNA in pathological mechanisms by subjecting H9C2 cells to 24-h formaldehyde exposure or administering formaldehyde (2.0 mg/kg) to female rats and examining their offspring. We indicate that lncRNA 91,234.1 (lnc91234) plays a role in FA-induced CHD by facilitating ferroptosis via PRMT1/ASCL4/GPX4 axis, which influences the methylation of H4R3, leading to lipid peroxidation and malondialdehyde (MDA) accumulation. This research is the first to demonstrate that exposure to FA disrupts cardiac function through ferroptosis and identifies lnc91234 as a novel lncRNA that may serve as a potential therapeutic target for cardiac dysplasia and CHD by modulating myocardial function both in vivo and in vitro.
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