Smoking Increases Inflammation and Metalloproteinase Expression in Human Carotid Atherosclerotic Plaques

Kangavari, Simon; Matetzky, Shlomo; Shah, Prediman K.; Yano, Juliana; Chyu, Kuang‐Yuh; Fishbein, Michael C.; Cercek, Bojan

doi:10.1177/107424840400900410

Cited by 42 publications

(27 citation statements)

References 26 publications

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“…96 Thus, smoking increases markers of inflammation and promotes plaque instability via multiple mechanisms of action; findings that may be correlated to the instability of atherosclerotic plaques in smokers. 97 …”

Section: Smokingmentioning

confidence: 99%

Inflammation at the Molecular Interface of Atherogenesis

Lamon

Hajjar

2008

The American Journal of Pathology

112

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Despite the multifactorial nature of atherosclerosis, substantial evidence has established inflammation as an often surreptitious, yet critical and unifying driving force which promotes disease progression. To this end, research has defined molecular networks initiated by cytokines, growth factors and other proinflammatory molecules which promote hallmarks of atherosclerosis such as endothelial dysfunction, macrophage infiltration, LDL oxidation, cell proliferation and thrombosis. Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. The agricultural, industrial and technological revolutions produced alterations in dietary, social and economic factors which have collectively exaggerated the exposure of the human genome to environmental stimuli. Furthermore, advances in sanitation, nutrition, and medicine have increased the lifespan of humans, effectively prolonging blood vessel exposure to these factors. As a result, the vasculature has become conditioned to respond to injury with what is arguably an overzealous immunological response; thus setting the stage for the prevalence of cardiovascular disease, including atherosclerotic plaque development in Western populations. Evidence suggests that each of these alterations can be linked to specific mediators in the inflammatory process. Integration of these factors with an inflammationbased hypothesis of atherosclerosis has yet to be extrapolated to observations in the realms of basic and clinical sciences and is the focus of this review. (Am J Pathol

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Section: Smokingmentioning

confidence: 99%

Inflammation at the Molecular Interface of Atherogenesis

Lamon

Hajjar

2008

The American Journal of Pathology

112

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“…107 Carotid endarterectomy specimens from cigarette smokers have higher MMP-12 and lower TIMP-1 expression than those from nonsmokers, and this is associated with decreased elastin content. 108 Variation in the stromeolysin-1 gene and smoking status demonstrated synergy in conferring risk for myocardial infarction. 109 …”

Section: Smoking and Regulation Of Matrix Metalloproteinase Activitymentioning

confidence: 99%

Smoking, Metalloproteinases, and Vascular Disease

Perlstein

Lee

2006

ATVB

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Abstract-Smoking causes up to 11% of total global cardiovascular deaths. Smoking has numerous effects that may promote atherosclerosis through vascular inflammation and oxidative stress, but the pathogenesis of smoking-related cardiovascular disease remains incompletely understood. The matrix metalloproteinases, a family of endopeptidases that can degrade extracellular matrix components in both physiological and pathophysiological states, play an important role in smoking-associated chronic obstructive pulmonary disease, the second leading cause of smoking attributable mortality. Emerging evidence indicates that the matrix metalloproteinases may also contribute to smoking-related vascular disease. Here we discuss the potential relationship between smoking, matrix metalloproteinases, and acceleration of vascular disease.

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“…33 Interestingly, the systemic proinflammatory effect of smoking is not limited to active smokers. Also patients exposed to secondhand smoke exhibit increased concentrations of inflammatory markers.…”

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confidence: 99%

Smoking and Cardiovascular Disease

Meßner

Bernhard

2014

ATVB

777

329

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Abstract-Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes. Clinical DataEvidence for smoking-induced initial vascular damage and endothelial dysfunction stems from an array of clinical studies analyzing endothelial function using various techniques. 6 As mentioned above, in 1993, Celermajer et al 5 were able to show that continuous smoking impairs FMD of the brachial artery in a dose-dependent manner, shown by the strong association between FMD and pack years smoked. This was also found to be the case with coronary arteries in a study by Zeiher et al. 7 Interestingly, reduction of endothelium-dependent dilatation by smoking was reversible, and significant improvement of FMD 1 year after cessation has been reported. 8 Likewise, a recent study of Amato et al 9 revealed that smoking light cigarettes impairs FMD as much as smoking regular cigarettes, arguing against light cigarettes as a less harmful alternative.Measurement of FMD represents a useful tool to assess the effects of smoking on the vascular wall. Independent of its FMD reducing activity, smoking was shown to induce other proatherogenic alterations in the vascular wall (eg, by deposition of smoke chemicals). The time needed to restore interrupted functions of the vascular endothelium will depend on the specific process that has caused the endothelial damage; some alterations of the endothelial wall may vanish more rapidly than others, without these being reflected by improved FMD.Clinical studies assessing the interrelation of secondhand smoking and FMD reported strong correlations. Secondhand smoking was shown to impair endo...

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Smoking Increases Inflammation and Metalloproteinase Expression in Human Carotid Atherosclerotic Plaques

Abstract: This study demonstrates that cigarette smoking increases markers of inflammation and tissue destruction in atherosclerotic plaques. This change in plaque composition may at least in part explain the effect of smoking on the instability of human atherosclerotic plaques.

Cited by 42 publications

References 26 publications

Inflammation at the Molecular Interface of Atherogenesis

Inflammation at the Molecular Interface of Atherogenesis

Smoking, Metalloproteinases, and Vascular Disease

Smoking and Cardiovascular Disease

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