Cardiovascular effects of carbon monoxide and cigarette smoking

Zevin, Shoshana; Saunders, Sandra; Gourlay, Steven G.; Jacob, Peyton; Benowitz, Neal L.

doi:10.1016/s0735-1097(01)01616-3

Cited by 137 publications

(94 citation statements)

References 47 publications

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“…However, CO at 250 ppm is well below the concentration of 3,000 ppm used in humans during measurement of diffusing capacity of the lung for CO (DL CO ) in pulmonary function testing. Furthermore, human and animal studies used CO concentration in the range of 250 ppm up to 1,500 ppm without adverse effects (27,42,55). CO is also generated endogenously in mammalian cells primarily as a major byproduct of heme degradation catalyzed by HO (33,45).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Wang¹,

Lee²,

Kwak³

et al. 2008

American Journal of Physiology-Renal Physiology

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Tubulointerstitial fibrosis is a hallmark of chronic progressive kidney disease leading to end-stage renal failure. An endogenous product of heme oxygenase activity, carbon monoxide (CO), has been shown to exert cytoprotection against tissue injury. Here, we explored the effects of exogenous administration of low-dose CO in an in vivo model of renal fibrosis induced by unilateral ureteral obstruction (UUO) and examined whether CO can protect against kidney injury. UUO in mice leads to increased extracellular matrix (ECM) deposition and tubulointerstitial fibrosis within 4 to 7 days. Kidneys of mice exposed to low-dose CO, however, had markedly reduced ECM deposition after UUO. Moreover, low-dose CO treatment inhibited the induction of α-smooth muscle actin (α-SMA) and major ECM proteins, type 1 collagen and fibronectin, in kidneys after UUO. In contrast, these anti-fibrotic effects of CO treatment were abrogated in mice carrying null mutation of Mkk3, suggesting involvement of the MKK3 signaling pathway in mediating the CO effects. Additionally, in vitro CO exposure markedly inhibited TGF-β1-induced expression of α-SMA, collagen, and fibronectin in renal proximal tubular epithelial cells. Our findings suggest that low-dose CO exerts protective effects, via the MKK3 pathway, to inhibit development of renal fibrosis in obstructive nephropathy.

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Section: Discussionmentioning

confidence: 99%

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Wang¹,

Lee²,

Kwak³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…So far there is only one study investigating the effect of CO on CRP level in 12 healthy smokers, with the result that CO administered under conditions similar to those of cigarette smoking had no significant effect on CRP (Zevin et al 2001). The present study is the first to demonstrate that hs-CRP is increased in subjects with chronic CO exposure.…”

Section: Present Findings Supporting Association Of Co Exposure With mentioning

confidence: 40%

“…This investigation is the first to assess and find an association between chronic CO exposure and CIMT and also is the second in the literature to assess the association between chronic CO exposure and hs-CRP levels and the first demonstrating an association (Zevin et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Chronic Carbon Monoxide Exposure Is Associated with the Increases in Carotid Intima-Media Thickness and C-Reactive Protein Level

Davutoğlu

Zengin

Sarı

et al. 2009

Tohoku J. Exp. Med.

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“…Despite of a great number of reports emphasizing that cardiovascular damage from cigarette smoking in both its forms, active and passive smoke, is an absolute certainty [1][2][3][4][5][6][7][8][9][10][11][12][13] , however debated opinions on the topic still exist primarily with regard to the type and reproducibility of damage, time of onset and progression of the lesions. In addition, a great question to be solved is whether once cardiovascular alterations begin are independent in their progression from smoking or, conversely, continue to need smoking compound effects.…”

Section: Introductionmentioning

confidence: 99%

Current and Controversial Features of Cardiovascular Damage from Cigarette Smoking

Leone

2016

Journal of Cardiology and Therapy

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A great number of studies have undoubtedly demonstrated that cardiovascular damage from cigarette smoking cannot be denied, although some controversies on the topic still exist. The damage to the heart and blood vessels is initially characterized by transient functional alterations consisting of endothelial dysfunction, reduced exercise tolerance, increased systolic blood pressure and heart rate following acute exposure. On the contrary, chronic exposure to smoking develops, at the time, firstly reversible and, then, irreversible lesions mainly involving myocardium with an ischemic damage and smoke cardiomyopathy as well as coronary, carotid and cerebral arteries, which display atherosclerotic pathology. The analysis of the epidemiological studies on cardiovascular damage support the controversies on the effects of smoking, because not the same alterations are sometimes observed in different studies on the topic. However, when standardized experimental procedures are followed, the same alterations are clearly reproduced showing that cardiovascular damage from cigarette smoking cannot be denied.

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Cardiovascular effects of carbon monoxide and cigarette smoking

Cited by 137 publications

References 47 publications

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Chronic Carbon Monoxide Exposure Is Associated with the Increases in Carotid Intima-Media Thickness and C-Reactive Protein Level

Current and Controversial Features of Cardiovascular Damage from Cigarette Smoking

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