ReviewActa Cardiologica Sinica2014
Nicotine: A Double-Edged Sword in Atherosclerotic Disease.
Review in Acta Cardiologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 12 citations in OpenAlex.
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- Exploring the association between melatonin and nicotine dependence (Review).International journal of molecular medicine · 2024Review
- Article
- Nicotine promotes vascular calcification via intracellular Ca2+-mediated, Nox5-induced oxidative stress, and extracellular vesicle release in vascular smooth muscle cells.Cardiovascular research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledChronic cigarette smoking is well-known to damage vascular endothelium, which initiates atherosclerosis by first manifesting as endothelial dysfunction and later progressing to cardiovascular diseases (CVD). Nicotine, a major component of tobacco smoke, is traditionally thought to be responsible for increased cardiovascular events through stimulation of the sympathetic nervous system, increased myocardial metabolic demand, impaired lipid metabolism, and activated platelet function. However, recent studies have demonstrated that nicotine, at lower doses, may be beneficial to the cardiovascular system. With binding to specific nicotinic acetylcholine receptors, nicotine can induce migration and proliferation of vascular cells, and hence enhances angiogenesis. Therefore, these seemingly inconsistent properties of nicotine may in fact give rise to novel and efficacious management strategies of CVD. KEY WORDS: Angiogenesis; Atherosclerosis; nicotinic acetylcholine receptors (nAChRs); Nicotine.
Identifiers
27122776PMC4805015W2181763161What 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.