The biology behind the atherothrombotic effects of cigarette smoke

  title={The biology behind the atherothrombotic effects of cigarette smoke},
  author={Adam Csord{\'a}s and David Bernhard},
  journal={Nature Reviews Cardiology},
Cigarette smoke is an aerosol that contains >4,000 chemicals, including nicotine, carbon monoxide, acrolein, and oxidant compounds. Exposure to cigarette smoke induces multiple pathological effects in the endothelium, several of which are the result of oxidative stress initiated by reactive oxygen species, reactive nitrogen species, and other oxidant constituents of cigarette smoke. Cigarette-smoke exposure interferes adversely with the control of all stages of plaque formation and development… 

Effects of Smoking on Oxidative Stress and Vascular Function

The role of endothelial dysfunction and its contributing factors, such as oxidative stress and inflammation, in the development of cardiovascular diseases are discussed and the studies which investigated the effect of tobacco and electronic smok - ing on the biomarkers of endotocyte dysfunction, stress, and inflammation are reported.

The Impact of Tobacco Cigarettes, Vaping Products and Tobacco Heating Products on Oxidative Stress

The impact of tobacco cigarette smoke on oxidative stress signaling in human health is well established, whereas the safety profile of MRPs seems to be higher than tobacco cigarettes, but further, well-conceived, studies are needed to better understand the oxidative effects of these products with long-term exposure.

Nicotine: regulatory roles and mechanisms in atherosclerosis progression.

  • Xiuxiu FuTingyu Zong Tao Yu
  • Biology, Medicine
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2021

Effect of Cigarette Smoke on Gut Microbiota: State of Knowledge

The current knowledge about the mechanistic interaction between cigarette smoke and intestinal microbiota dysbiosis is reviewed, the likely actions of nicotine, aldehydes, polycyclic aromatic hydrocarbons, heavy metals, volatile organic compounds and toxic gases are reviewed, and the potential mechanisms of the lung–gut cross talk and skin-gutcross talk in regulating the balance of intestinal microbiota are revealed.

Exposure to Cigarette Smoke Augments Post-ischemic Brain Injury and Inflammation via Mobilization of Neutrophils and Monocytes

It is reported that exposure to cigarette smoke exacerbated ischemic brain injury in mice subjected to transient middle cerebral artery occlusion (MCAO), and it is suggested that cigarette smoke-induced mobilization of peripheral neutrophils and monocytes augments ischeic brain injury.

Effects of Exposure to Tobacco Cigarette, Electronic Cigarette and Heated Tobacco Product on Adipocyte Survival and Differentiation In Vitro

It is demonstrated that CS extract, in contrast to HTP and ECIG extracts, significantly impairs differentiation of pre-adipocytes to beige adipocytes and may therefore impact significantly adipose tissue metabolic function.

Protection from cigarette smoke‐induced vascular injury by recombinant human relaxin‐2 (serelaxin)

It is demonstrated that RLX is capable of counteracting CS‐mediated vascular damage and dysfunction by reducing oxidative stress, thus adding a tile to the growing mosaic of the beneficial effects of RLX in CVD.

Cigarette smoke-induced oxidative stress activates NRF2 to mediate fibronectin disorganization in vascular formation

This work shows that cigarette smoke extract (CSE)-induced oxidative stress disturbs fibronectin (FN) assembly during angiogenesis and demonstrates the cardiovascular dysfunction caused by CSE from a novel perspective that NRF2-dependent signalling engages in FN disorganization.



The pathophysiology of cigarette smoking and cardiovascular disease: an update.

Cigarette Smoke Impairs Endothelial Cell Prostacyclin Production

This in vitro study shows that impairment of an endothelial cell function is related to a risk factor for atherosclerosis.

Structural and functional alteration of blood vessels caused by cigarette smoking: an overview of molecular mechanisms.

Findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter.

Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

DSP induces cerebral vessel inflammation with activation of p38 MAPK inflammatory signal and the downstream transcriptional factors (ATF-2 and Elk-1) in parallel with enhanced extracellular-matrix-related gene transcription and increased AT1 receptor expression in the cerebral arteries, which are key events in stroke pathogenesis.

Relevance of endothelial-haemostatic dysfunction in cigarette smoking.

Evidence that loss of normal endothelial function may result in a loss of the balance of the haemostatic system and in changes of the platelet physiology that may be relevant for the pathogenic effect of smoking on the development of atherothrombosis is reviewed.

Effect of a cigarette smoke extract on the metabolism of the proinflammatory autacoid, platelet-activating factor.

The increase of PAF may contribute to the increased incidence of cardiovascular and lung diseases known to be present in smokers and may account for the increase in the plasma PAF concentration that is known to occur in smokers.

Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice.

This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases and led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease.