Why the study?
Maternal exposure to PM2.5 is associated with congenital heart defects in fetuses, but the exact mechanisms remain unclear.
Does gestational exposure to PM2.5 impair cardiac development through ANGPTL4-mediated mitochondrial metabolic dysfunction?
Population
Human umbilical cord serum samples, offspring mice, and cardiomyocytes
Comparison
Maternal or in vitro PM2.5 exposure vs unexposed controls
Design
Preclinical in vivo and in vitro mechanistic study
Key result
Maternal exposure to PM2.5 impaired cardiac development and induced mitochondrial dysfunction in offspring through an ANGPTL4-mediated pathway.
Authors
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Hypothesis-generating for ANGPTL4/SIRT3 biomarkers in maternal PM2.5-related CHD; prospective studies needed before clinical adoption.
Does gestational exposure to PM2.5 impair cardiac development through ANGPTL4-mediated mitochondrial metabolic dysfunction?
Maternal exposure to PM2.5 impairs fetal cardiac development via ANGPTL4-mediated mitochondrial dysfunction, providing a mechanistic basis for PM2.5-related congenital heart defects.
Lv et al. (2025) studied Congenital heart defects. Maternal exposure to PM2.5 was evaluated on Cardiac development and mitochondrial function. Maternal exposure to PM2.5 impaired cardiac development and induced mitochondrial dysfunction in offspring through an ANGPTL4-mediated pathway.