Nicotine Induces Fetal Cardiac Dysfunction by Promoting Cardiomyocyte Apoptosis Through Regulating the KCTD10-Notch Signaling
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View abstract on PubMed
Summary
This summary is machine-generated.Maternal nicotine exposure (MNE) harms fetal heart development by increasing cardiomyocyte apoptosis via the KCTD10-Notch pathway, leading to cardiac dysfunction.
Area Of Science
- Cardiology
- Developmental Biology
- Toxicology
Background
- Congenital heart defects (CHD) are a significant cause of cardiac dysfunction.
- Maternal smoking during pregnancy is a known risk factor for CHD.
- Nicotine, a primary component of tobacco smoke, is suspected to contribute to these defects.
Purpose Of The Study
- To investigate the impact of maternal nicotine exposure (MNE) on fetal cardiac dysfunction in a mouse model.
- To elucidate the underlying molecular mechanisms by which nicotine affects fetal heart development.
- To explore the role of the KCTD10-Notch pathway in nicotine-induced cardiac dysfunction.
Main Methods
- Maternal mice were exposed to nicotine, and pregnancy outcomes were assessed.
- Fetal cardiac function, weight, and placental weight were measured.
- Primary cardiomyocytes were isolated for in vitro analysis of apoptosis and inflammation.
- Molecular mechanisms were studied using molecular docking, qPCR, and Western blotting.
- The Notch pathway was pharmacologically inhibited using DAPT.
Main Results
- MNE led to reduced fetal weight, impaired cardiac function, and decreased maternal pregnancy rates.
- Nicotine exposure in vitro induced apoptosis and inflammation in cardiomyocytes.
- Nicotine decreased KCTD10 expression and activated the Notch pathway.
- Inhibition of the Notch pathway with DAPT ameliorated nicotine-induced cardiomyocyte injury and MNE-related fetal cardiac dysfunction.
Conclusions
- Nicotine exposure during pregnancy may promote fetal cardiac dysfunction.
- This dysfunction appears to be mediated by increased cardiomyocyte apoptosis.
- The KCTD10-Notch signaling pathway is implicated in the mechanism of nicotine-induced fetal cardiac defects.
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