Evidence map›Paper›PMID 35521669›Full record

ArticleJournal of cellular and molecular medicine2022

Maternal nicotine exposure induces congenital heart defects in the offspring of mice.

Elizabeth R Greco, Anish Engineer, Tana Saiyin, Xiangru Lu, MengQi Zhang, Douglas L Jones, Qingping Feng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Prenatal Cannabis and Tobacco: Studies in Animal Models.Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Maternal Immune Activation: Implications for Congenital Heart Defects.Clinical reviews in allergy & immunology · 2025
    Review
  7. Developmental nicotine exposure alters cardiovascular structure and function in neonatal and juvenile rats.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  8. Article
  9. Article
  10. An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024
    Review
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Elizabeth R GrecoDepartment of Physiology and Pharmacology, London, Ontario, Canada.
Anish EngineerDepartment of Physiology and Pharmacology, London, Ontario, Canada.
Tana SaiyinDepartment of Physiology and Pharmacology, London, Ontario, Canada.
Xiangru LuDepartment of Physiology and Pharmacology, London, Ontario, Canada.
MengQi ZhangDepartment of Physiology and Pharmacology, London, Ontario, Canada.
Douglas L JonesDepartment of Physiology and Pharmacology, London, Ontario, Canada.
Qingping FengDepartment of Physiology and Pharmacology, London, Ontario, Canada.ORCID 0000-0001-9739-2765
London Health Sciences Centre · CAWestern University · CA

Funding

CIHR
6 · The paper itself

Abstract

Maternal cigarette smoking is a risk factor for congenital heart defects (CHDs). Nicotine replacement therapies are often offered to pregnant women following failed attempts of smoking cessation. However, the impact of nicotine on embryonic heart development is not well understood. In the present study, the effects of maternal nicotine exposure (MNE) during pregnancy on foetal heart morphogenesis were studied. Adult female mice were treated with nicotine using subcutaneous osmotic pumps at 0.75 or 1.5 mg/kg/day and subsequently bred with male mice. Our results show that MNE dose-dependently increased CHDs in foetal mice. CHDs included atrial and ventricular septal defects, double outlet right ventricle, unguarded tricuspid orifice, hypoplastic left ventricle, thickened aortic and pulmonary valves, and ventricular hypertrophy. MNE also significantly reduced coronary artery size and vessel abundance in foetal hearts. Moreover, MNE resulted in higher levels of oxidative stress and altered the expression of key cardiogenic regulators in the developing heart. Nicotine exposure reduced epicardial-to-mesenchymal transition in foetal hearts. In conclusion, MNE induces CHDs and coronary artery malformation in mice. These findings provide insight into the adverse outcomes of foetuses by MNE during pregnancy.

Indexed as

Heart Defects, CongenitalPrenatal Exposure Delayed EffectsSmoking CessationAnimalsFemaleHumansMaleMiceNicotinePregnancyTobacco Use Cessation DevicesNicotinecongenital heart defectsembryonic heart developmentmaternal nicotine exposurenicotine replacement therapy

Identifiers

PMID35521669
PMCPMC9170818
OpenAlexW4229067668

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.