Key result
Perinatal nicotine exposure induces excessive cardiac collagen deposition through MIAT induction, increasing the predisposition to cardiac dysfunction in offspring.
Perinatal nicotine exposure increases cardiac collagen deposition via MIAT induction, providing a mechanistic basis for the predisposition to cardiac dysfunction in exposed offspring.
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Supports caution on maternal nicotine for offspring cardiac outcomes; leaves open translation beyond this animal model.
Using an established rat model and cultured primary neonatal cardiac fibroblasts, we show that nicotine mediated MIAT induction as the underlying mechanism for the excessive cardiac collagen deposition. These observations provide mechanistic basis for the increased predisposition to cardiac dysfunction following perinatal cigarette/nicotine exposure and offer novel potential therapeutic targets.
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Chuang et al. (2020) studied this question. Perinatal nicotine exposure induces excessive cardiac collagen deposition through MIAT induction, increasing the predisposition to cardiac dysfunction in offspring.
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