ArticleHypertension (Dallas, Tex. : 1979)2024
Prenatal Nicotine Exposure Raises Male Blood Pressure via FTO-Mediated NOX2/ROS Signaling.
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- FTO Deficiency Inhibits Vascular Endothelial Cell Apoptosis and Improved Mitophagy in Obesity-Related Hypertension by Enhancing NDRG1 m6A Methylation.Biochemical genetics · 2026Article
- FTO/m6A Regulate Prenatal Nicotine-Induced eNOS Uncoupling and BP Susceptibility.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Article
- Maternal-Fetal Crosstalk in Cardiovascular Programming: Linking the Intrauterine Environment to Lifelong Disease Risk.Journal of cardiovascular development and disease · 2026Review
- Nicotine promotes cardiac fibrosis by regulating miR-125b-5p maturation via HNRNPA2B1-mediated METTL14-dependent m⁶A methylation: therapeutic reversal by cinacalcet HCl.Journal of translational medicine · 2026Article
- DNA Methylation and Fetal Programming of Cardiovascular Disease: From Congenital Heart Diseases to Adult Cardiovascular Dysfunction.Reviews in cardiovascular medicine · 2026Review
- FTO-dependent m6A methylation mediates gestational diabetes mellitus-induced offspring cardiac senescent hypertrophy and dysfunction.iScience · 2026Article
- Decoding the role of mNeurochemistry international · 2025Review
- Cocoa Shell Extract Restores Redox Balance in Developmental Hypertension in Male Rats: Roles of Nrf2, SOD2 and p-eNOS.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- 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
- METTL14-mediated upregulation of lncRNA HOTAIR represses PP1α expression by promoting H3K4me1 demethylation in oxycodone-treated mice.CNS neuroscience & therapeutics · 2024Article
- Smoked, smokeless, and poly-tobacco use during pregnancy in relation to infant mortality in Cambodia: Findings from a nationwide sample.Tobacco induced diseases · 2024Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCigarette smoking/nicotine exposure in pregnancy shows an increased risk of hypertension in offspring, but the mechanisms are unclear. This study tested the hypothesis that m6A RNA hypomethylation epigenetically regulates vascular NOX (NADPH oxidase) and reactive oxygen species production, contributing to the fetal programming of a hypertensive phenotype in nicotine-exposed offspring.
methodsPregnant rats were exposed to episodic chronic intermittent nicotine aerosol (CINA) or saline aerosol control from gestational day 4 to day 21, and experiments were performed in 6-month-old adult offspring.
resultsAntenatal CINA exposure augmented Ang II (angiotensin II)-stimulated blood pressure response in male, but not female offspring. Moreover, CINA increased vascular NOX2 expression and superoxide production exclusively in male offspring. Inhibition of NOX2 with gp91ds-tat, both ex vivo and in vivo, mitigated the CINA-induced elevation in superoxide production and blood pressure response. Notably, CINA enhanced the expression of vascular m6A demethylase FTO (fat mass and obesity-associated protein), while reducing the total vascular m6A abundance and specific m6A methylation of the NOX2 gene. Additionally, ex vivo inhibition of FTO with FB23-2 attenuated CINA-induced increases in vascular NOX2 expression. In vitro experiments using human umbilical vein endothelial cells demonstrated that nicotine dose-dependently upregulated FTO and NOX2 protein abundance, which were reversed by treatment with the FTO inhibitor FB23-2 or FTO knockdown using siRNAs.
conclusionsThis study uncovers a new mechanism: m6A demethylase FTO-mediated epigenetic upregulation of vascular NOX2 signaling in CINA-induced hypertensive phenotype. This insight could lead to a therapeutic target for preventing and treating developmental hypertension programming.
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