Statins attenuate the development of atherosclerosis and endothelial dysfunction induced by exposure to urban particulate matter (PM10)

Miyata, Ryohei; Hiraiwa, Kunihiko; Cheng, Jui Chih; Bai, Na; Vincent, Renaud; Francis, Gordon A.; Sin, Don D.; Eeden, Stephan F. van

doi:10.1016/j.taap.2013.05.033

Cited by 30 publications

(18 citation statements)

References 33 publications

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“…It is known that PM10 exposure increases plasma ET-1 levels [56], thus mediating systemic endothelial dysfunction. We demonstrated also PM10sum toxicity on cardiovascular system and brain parenchyma after PM10sum instillation, thus confirming PM systemic effects [24].…”

Section: Discussionmentioning

confidence: 99%

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

et al. 2014

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Adverse health effects of air pollution attributed mainly to airborne particulate matter have been well documented in the last couple of decades. Short term exposure, referring to a few hours exposure, to high ambient PM10 concentration is linked to increased hospitalization rates for cardiovascular events, typically 24 h after air pollution peaks. Particulate matter exposure is related to pulmonary and cardiovascular diseases, with increased oxidative stress and inflammatory status. Previously, we have demonstrated that repeated intratracheal instillation of PM10sum in BALB/c mice leads to respiratory tract inflammation, creating in lung a condition which could potentially evolve in a systemic toxic reaction. Additionally, plasma membrane and tissue lipids are easily affected by oxidative stress and directly correlated with inflammatory products. With this aim, in the present investigation using the same model, we analyzed the toxic potential of PM10sum exposure on lipid plasma membrane composition, lipid peroxidation and the mechanisms of cells protection in multiple organs such as lung, heart, liver and brain. Obtained results indicated that PM10 exposure led to lung lipid reshaping, in particular phospholipid and cholesterol content increases; concomitantly, the generation of oxidative stress caused lipid peroxidation. In liver we found significant changes in lipid content, mainly due to an increase of phosphatidylcholine, and in total fatty acid composition with a more pronounced level of docosahexaenoic acid; these changes were statistically correlated to lung molecular markers. Heart and brain were similarly affected; heart was significantly enriched in triglycerides in half of the PM10sum treated mice. These results demonstrated a direct involvement of PM10sum in affecting lipid metabolism and oxidative stress in peripheral tissues that might be related to the serious systemic air-pollution effects on human health.

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Section: Discussionmentioning

confidence: 99%

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

et al. 2014

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“…Beta-blockers or antagonists of alveolar sensory receptors can attenuate the cardiac effects of C-DEAP in rodent models (177,234). Additionally, endothelin receptor antagonists (175,235), inhibitors of the renin/angiotensin system (236), and statins (237,238) can reduce the vascular and atherosclerotic effects of air pollutants.…”

Section: Role Of Oxidative Stress In the Cardiovascular Effects Of Aimentioning

confidence: 99%

Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution

Niemann

Rohrbach

Miller

et al. 2017

Journal of the American College of Cardiology

281

177

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Oxidative stress occurs whenever the release of reactive oxygen species (ROS) exceeds endogenous antioxidant capacity. In this paper, we review the specific role of several cardiovascular risk factors in promoting oxidative stress, namely diabetes, obesity, smoking, and excessive pollution. Specifically, the risk of developing heart failure is higher in patients with diabetes or obesity, even with optimal medical treatment, and the increased release of ROS from cardiac mitochondria and other sources likely contributes to the development of cardiac dysfunction in this setting. Here, we explore the role of different ROS sources arising in obesity and diabetes, and the impact of excessive ROS production on the development of cardiac lipotoxicity. In parallel, contaminants in the air that we breathe pose a significant threat to human health. This paper provides an overview of cigarette smoke and urban air pollution, considering how their composition and biological effects have detrimental effects on cardiovascular health.

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“…The translocation of eNOS to the intracellular structures may be responsible for the increased peroxynitrite formation. The authors hypothesized that lipophilic HMGR inhibitors may promote oxidative stress (36). Endothelium-derived NO is an important mediator of endothelial function, and several mechanisms have been reported for the upregulation of eNOS by statins (35).…”

Section: Discussionmentioning

confidence: 99%

Effect of rosuvastatin on hyperuricemic rats and the protective effect on endothelial dysfunction

Xilifu

Abudula

Rehemu

et al. 2014

Experimental and Therapeutic Medicine

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Endothelial dysfunction plays a key role in the development of cardiovascular diseases, renal injuries and hypertension induced by hyperuricemia. Therapies targeting uric acid (UA) may be beneficial in cardiovascular diseases. In the present study, the effect of rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, was investigated to determine whether rosuvastatin improves endothelial dysfunction via the endothelial nitric oxide (NO) pathway and delays the pathogenesis of endothelial dysfunction in hyperuricemic rats. A total of 72 Sprague-Dawley rats (age, 8 weeks) were randomly divided into six groups (12 rats per group), including the control, model, 2.5 mg/kg/day rosuvastatin, 5 mg/kg/day rosuvastatin, 10 mg/kg/day rosuvastatin and 53.57 mg/kg/day allopurinol groups. The model, rosuvastatin and allopurinol rats were subjected to hyperuricemia, induced by the administration of yeast extract powder (21 g/kg/day) and oxonic acid potassium salt (200 mg/kg/day). The hyperuricemic rats were treated with 2.5, 5.0 or 10.0 mg/kg/day rosuvastatin orally for six weeks, while rats treated with allopurinol (53.57 mg/kg/day) were used as a positive control. The serum levels of NO and the gene expression levels of endothelial NO synthase in the aortic tissue increased, whereas the serum levels of UA, endothelin-1 and angiotensin II decreased in the hyperuricemic rats treated with rosuvastatin, particularly at a high rosuvastatin dose (10 mg/kg/day). In addition, the curative effect of the 10 mg/kg/day rosuvastatin group was evidently higher compared with the allopurinol group. Therefore, rosuvastatin may be a novel drug candidate for the treatment of hyperuricemia due to its endothelial protective properties.

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Statins attenuate the development of atherosclerosis and endothelial dysfunction induced by exposure to urban particulate matter (PM10)

Cited by 30 publications

References 33 publications

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution

Effect of rosuvastatin on hyperuricemic rats and the protective effect on endothelial dysfunction

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