ArticleJournal of cellular and molecular medicine2018
Nicotine induces endothelial dysfunction and promotes atherosclerosis via GTPCH1.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Physiological influences on neurovascular coupling: A systematic review of multimodal imaging approaches and recommendations for future study designs.Experimental physiology · 2025Pooled it
- Atherogenic Effects of Acute Electronic Cigarette Compared With Tobacco Cigarette Smoking in People Living With HIV: A Randomized Crossover Trial.Journal of the American Heart Association · 2025Trial
- Nicotine-containing products and the cardiovascular system: mechanisms and global health implications.Nature reviews. Cardiology · 2026Review
- Nicotine-Mediated Redox and Nitrosative Stress in Cardiorenal Health.Hypertension (Dallas, Tex. : 1979) · 2026Review
- Nicotine as a cardiovascular drug: haemodynamic stress, oxidative injury, and the regulatory failure to protect the heart.European heart journal open · 2026Article
- Exploring the therapeutic synergy of drug-lifestyle interventions in fluorosis: a randomized trial on cardiovascular metabolic outcomes from the China fluorosis cohort (CFC).Frontiers in pharmacology · 2026Article
- A novel redox signalling axis mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2026Article
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- Coronary artery spasm: mechanisms, risk factors, and translational strategies for precision management.Frontiers in cardiovascular medicine · 2026Review
- Exploring the Impact of E-cigarettes on Cardiovascular Health: Insights from Preclinical and Clinical Studies.Cardiovascular toxicology · 2025Review
- Multifaceted Nature of HuR in Atherosclerosis Development.Current medicinal chemistry · 2025Review
- An adverse outcome pathway for cigarette smoke-mediated oxidative stress in plaque formation.Frontiers in toxicology · 2025Review
- Article
- Cardiovascular Risk Factors as Independent Predictors of Diabetic Retinopathy in Type II Diabetes Mellitus: The Development of a Predictive Model.Medicina (Kaunas, Lithuania) · 2024Article
- Citronellal improves endothelial dysfunction by affecting the stability of the GCH1 protein.Acta biochimica et biophysica Sinica · 2024Article
- Acute cardiovascular effects of 4th generation electronic cigarettes and combusted cigarettes: implications for harm reduction.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Arterial Stiffness and Carotid Intima-Media Thickness in Children Exposed to Smokeless Tobacco in Fetal Life.Journal of the American Heart Association · 2024Article
- The Role of Microglia in Sex- and Region-Specific Blood-Brain Barrier Integrity During Nicotine Withdrawal.Biological psychiatry global open science · 2024Article
- Vascularized liver-on-a-chip model to investigate nicotine-induced dysfunction.Biomicrofluidics · 2023Article
- A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smoking is a major preventable risk factor for atherosclerosis. However, the causative link between cigarette smoke and atherosclerosis remains to be established. The objective of this study is to characterize the role of GTP cyclohydrolase 1 (GTPCH1), the rate-limiting enzyme for de novo tetrahydrobiopterin (BH4) synthesis, in the smoking-accelerated atherosclerosis and the mechanism involved. In vitro, human umbilical vein endothelial cells were treated with nicotine, a major component of cigarette smoke, which reduced the mRNA and protein levels of GTPCH1 and led to endothelial dysfunction. GTPCH1 overexpression or sepiapterin could attenuate nicotine-reduced nitric oxide and -increased reactive oxygen species levels. Mechanistically, human antigen R (HuR) bound with the adenylateuridylate-rich elements of the GTPCH1 3' untranslated region and increased its stability; nicotine inhibited HuR translocation from the nucleus to cytosol, which downregulated GTPCH1. In vivo, nicotine induced endothelial dysfunction and promoted atherosclerosis in ApoE
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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.