ArticlePloS one2016
Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- In utero chronic intermittent nicotine aerosol exposure increases ischemic heart injury in adult offspring via programming of Angiotensin II receptor-derived TGFβ/ROS/Akt signaling pathway.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease.Frontiers in pharmacology · 2023Review
- Methamphetamine Use During the First or Second Half of Pregnancy Worsens Cardiac Ischemic Injury in Adult Female Offspring.Physiological research · 2022Article
- Prenatal Exposure to Methamphetamine Causes Vascular Dysfunction in Adult Male Rat Offspring.Frontiers in cardiovascular medicine · 2022Article
- Assessment of Cardiovascular Health of Children Ages 6 to 10 Years Conceived by Assisted Reproductive Technology.JAMA network open · 2021Article
- Gasotransmitters for the Therapeutic Prevention of Hypertension and Kidney Disease.International journal of molecular sciences · 2021Review
- Animal Models for DOHaD Research: Focus on Hypertension of Developmental Origins.Biomedicines · 2021Review
- Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target?Antioxidants (Basel, Switzerland) · 2021Review
- Adverse effects of fetal exposure of electronic-cigarettes and high-fat diet on male neonatal hearts.Experimental and molecular pathology · 2021Article
- Does Prenatal Exposure to CNS Stimulants Increase the Risk of Cardiovascular Disease in Adult Offspring?Frontiers in cardiovascular medicine · 2021Review
- Mechanism underlying increased cardiac extracellular matrix deposition in perinatal nicotine-exposed offspring.American journal of physiology. Heart and circulatory physiology · 2020Article
- Early Life Oxidative Stress and Long-Lasting Cardiovascular Effects on Offspring Conceived by Assisted Reproductive Technologies: A Review.International journal of molecular sciences · 2020Review
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- Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions.International journal of biological sciences · 2020Article
- Epigenetic down-regulation of BKInternational journal of cardiology · 2019Article
- Epigenetic Down-Regulation of Sirt 1 via DNA Methylation and Oxidative Stress Signaling Contributes to the Gestational Diabetes Mellitus-Induced Fetal Programming of Heart Ischemia-Sensitive Phenotype in Late Life.International journal of biological sciences · 2019Article
- Antioxidant role of melatonin against nicotine's teratogenic effects on embryonic bone development.Iranian journal of basic medical sciences · 2018Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Role of DNA methylation in perinatal nicotine-induced development of heart ischemia-sensitive phenotype in rat offspring.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Fetal nicotine exposure increased risk of developing cardiovascular disease later in life. The present study tested the hypothesis that perinatal nicotine-induced programming of heart ischemia-sensitive phenotype is mediated by enhanced reactive oxygen species (ROS) in offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth, in the absence or presence of a ROS inhibitor, N-acetyl-cysteine (NAC) in drinking water. Experiments were conducted in 8 month old age male offspring. Isolated hearts were perfused in a Langendorff preparation. Perinatal nicotine treatment significantly increased ischemia and reperfusion-induced left ventricular injury, and decreased post-ischemic recovery of left ventricular function and coronary flow rate. In addition, nicotine enhanced cardiac ROS production and significantly attenuated protein kinase Cε (PKCε) protein abundance in the heart. Although nicotine had no effect on total cardiac glycogen synthase kinase-3β (GSK3β) protein expression, it significantly increased the phosphorylation of GSK3β at serine 9 residue in the heart. NAC inhibited nicotine-mediated increase in ROS production, recovered PKCε gene expression and abrogated increased phosphorylation of GSK3β. Of importance, NAC blocked perinatal nicotine-induced increase in ischemia and reperfusion injury in the heart. These findings provide novel evidence that increased oxidative stress plays a causal role in perinatal nicotine-induced developmental programming of ischemic sensitive phenotype in the heart, and suggest potential therapeutic targets of anti-oxidative stress in the treatment of ischemic heart disease.
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Registered trials
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.