ArticleVascular health and risk management2021
Early Detection of Negative Smoking Impacts: Vascular Adaptation Deviation Based on Quantification of Circulated Endothelial Activation Markers.
Article in Vascular health and risk management, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07316400 (Protocol for a Randomized, Single-Blind, Controlled Clinical Trial Evaluating the Effect of Peptide Polysaccharide Supplementation on Serum Malondialdehyde, Interleukin-6, and Cotinine Levels), which is not on this map. Cited by 3 papers.
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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.
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.
Protocol for a Randomized, Single-Blind, Controlled Clinical Trial Evaluating the Effect of Peptide Polysaccharide Supplementation on Serum Malondialdehyde, Interleukin-6, and Cotinine Levels
Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- E-selectin, but not CRP, partially mediates the association between metabolic indices and insulin resistance in older adults: a mediation analysis.Asian biomedicine : research, reviews and news · 2026Article
- Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis.Tobacco induced diseases · 2024Article
- Detection of Vascular Inflammation and Oxidative Stress by Cotinine in Smokers: Measured Through Interleukin-6 and Superoxide Dismutase.International journal of general medicine · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSmoking can cause vascular damage in the form of an inflammatory reaction characterized by endothelial activation. Endothelial activation forms a pathological adaptation pattern so that it can induce the atherogenesis process. Several markers, such as E-selectin, platelet-derived micro particles (PMPs) and hematopoietic stem cell (HSC) can identify the activation of endothelial in circulating blood. Therefore, the deviation of vascular adaptation due to smoking can be detected early through the feedback mechanism between E-selectin, PMPs, and HSC. PURPOSE: This study aims to analyze the initial picture of the negative impact of smoking on vascular adaptation by measuring E-selectin, PMPs, and HSC in the peripheral blood circulation. Participant criteria and methods: Peripheral blood samples (5 mL) were taken from each participant, both the smoking group (n = 30) and the non-smoker group (n = 31) to obtain peripheral blood mononuclear cells (PBMNC). PBMNC was isolated using ficoll-based gradient centrifugation. The flow cytometry assay method used to measure the E-selectin, PMPs and hematopoietic stem cells.
resultsThe mean of circulating E-selectin in smokers was higher than that of non-smokers. On the other hand, the average number of PMPs and HSCs in smokers was lower than non-smokers.
conclusionSmoking increases the risk of accelerated vascular block formation, as indicated by an increase in the amount of circulating E-selectin. The increase in E-selectin in the blood vessels mediates the increased adhesion of PMPs in the vascular area so that the number of circulating PMPs in smokers decreases. The decrease in circulating PMPs decreases the signal of vascular repair, which is characterized by a decline in the number of HSCs.
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