ReviewMutation research2007
The role of tobacco smoke induced mitochondrial damage in vascular dysfunction and atherosclerosis.
Review in Mutation research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- An updated meta-analysis showed smoking modify the association of GSTM1 null genotype on the risk of coronary heart disease.Bioscience reports · 2021Pooled it
- ANT1 Deficiency Impairs Macrophage Metabolism and Migration, Protecting Against Emphysema in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Underpinnings of heart failure with preserved ejection fraction in women - From prevention to improving function. A co-publication with the American Journal of Preventive Cardiology and the Journal of Cardiac Failure.American journal of preventive cardiology · 2025Article
- Impact of Tobacco Consumption on Salivary Protein Profiles: A MALDI-TOF Mass Spectrometry Study.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- Mitochondrial Dysfunction and Risk Factors for Noncommunicable Diseases: From Basic Concepts to Future Prospective.Diseases (Basel, Switzerland) · 2024Review
- Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Cigarette Smoking, Cessation, and Risk of Heart Failure With Preserved and Reduced Ejection Fraction.Journal of the American College of Cardiology · 2022Article
- SUL-151 Decreases Airway Neutrophilia as a Prophylactic and Therapeutic Treatment in Mice after Cigarette Smoke Exposure.International journal of molecular sciences · 2021Article
- Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Pod-based menthol and tobacco flavored e-cigarettes cause mitochondrial dysfunction in lung epithelial cells.Toxicology letters · 2020Article
- Comparison of the cardiac effects of electronic cigarette aerosol exposure with waterpipe and combustible cigarette smoke exposure in rats.Life sciences · 2020Article
- A Mitochondrial Specific Antioxidant Reverses Metabolic Dysfunction and Fatty Liver Induced by Maternal Cigarette Smoke in Mice.Nutrients · 2019Article
- Mitochondrial toxicity of tobacco smoke and air pollution.Toxicology · 2017Review
- Lung epithelial response to cigarette smoke and modulation by the nicotinic alpha 7 receptor.PloS one · 2017Article
- Review
- In Silico Investigation of Traditional Chinese Medicine for Potential Lead Compounds as SPG7 Inhibitors against Coronary Artery Disease.Molecules (Basel, Switzerland) · 2016Article
- An In Vitro Study of the Neurotoxic Effects of N-Benzylpiperazine: A Designer Drug of Abuse.Neurotoxicity research · 2016Article
- Particulate matter and atherosclerosis: a bibliometric analysis of original research articles published in 1973-2014.BMC public health · 2016Review
- Mitochondrial functional impairment in response to environmental toxins in the cardiorenal metabolic syndrome.Archives of toxicology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The majority of individuals chronically exposed to tobacco smoke will eventually succumb to cardiovascular disease (CVD). However, despite the major cardiovascular health implications of tobacco smoke exposure, concepts of how such exposure specifically results in cardiovascular cell dysfunction that leads to CVD development are still being explored. Moreover, surprisingly little is known about the effects of prenatal and childhood tobacco smoke exposure on adult CVD development. Herein, it is proposed that the mitochondrion is a central target for environmental oxidants, including tobacco smoke. By virtue of its multiple, essential roles in cell function including energy production, oxidant signaling, apoptosis, immune response, and thermogenesis, damage to the mitochondrion will likely play an important role in the development of multiple common forms of human disease, including CVD. Specifically, this review will discuss the potential role of tobacco smoke and environmental oxidant exposure in the induction of mitochondrial damage which is related to CVD development. Furthermore, mechanisms of how mitochondrial damage can initiate and/or contribute to CVD are discussed, as are experimental results that are consistent with the hypothesis that mitochondrial damage and dysfunction will increase CVD susceptibility. Aspects of both adult and developmental (fetal and childhood) exposure to tobacco smoke on mitochondrial damage, function and disease development are also discussed, including the future implications and direction of studies involving the role of the mitochondrion in influencing disease susceptibility mediated by environmental factors.
Indexed as
Identifiers
What OpenQuestion holds
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.