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Open AccessJournal ArticleDOI

Nicotine Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells

TLDR
Activation of &agr;7 nicotinic acetylcholine receptor on MCs is a mechanism by which nicotine enhances atherosclerosis.
Abstract
Objective—Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The ...

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Citations
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Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis.

TL;DR: It is found that nicotine resulted in larger atherosclerotic plaques and secretion of inflammatory cytokines in ApoE−/− mice fed with a high-fat diet (HFD) and pyroptosis is likely a cellular mechanism for the pro-atherosclerosis property of nicotine.
Journal ArticleDOI

Nicotine-mediated autophagy of vascular smooth muscle cell accelerates atherosclerosis via nAChRs/ROS/NF-κB signaling pathway

TL;DR: Nicotine-induced autophagy promotes the phenotype switching of VSMCs and accelerates atherosclerosis, which is partly mediated by the nAChRs/ROS/NF-κB signaling pathway.
Journal ArticleDOI

Leptin increases mitochondrial OPA1 via GSK3-mediated OMA1 ubiquitination to enhance therapeutic effects of mesenchymal stem cell transplantation.

TL;DR: In the hostile microenvironment caused by MI, leptin can maintain the mitochondrial integrity and prolong the survival of hMSCs; leptin-mediated mitochondrial integrity requires phosphorylation of GSK3 as a prerequisite for ubiquitination-depended degradation of OMA1 and attenuation of long-OPA1 cleavage.
References
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Journal ArticleDOI

Inflammation in atherosclerosis

TL;DR: The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.
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The pathophysiology of cigarette smoking and cardiovascular disease: An update

TL;DR: Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction.
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Pathology of the Vulnerable Plaque

TL;DR: Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated and the non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA).
Journal ArticleDOI

Integrated signalling pathways for mast-cell activation

TL;DR: How the capacity of KIT, and other receptors, to influence FcεRI-dependent mast-cell-mediator release might be a function of the relative abilities of these receptors to activate these alternative pathways is described.
Journal ArticleDOI

Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis

TL;DR: In mouse models of lung cancer and atherosclerosis, it was found that nicotine enhanced lesion growth in association with an increase in lesion vascularity, and these effects were mediated through nicotinic acetylcholine receptors at nicotine concentrations that are pathophysiologically relevant.
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