aortic aneurysm/nikotiin

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Nicotine-stimulated elastase activity release by neutrophils in patients with abdominal aortic aneurysms.

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Elevated elastase activity in patients with chronic obstructive pulmonary disease (COPD) is attributable to the direct effect of nicotine. COPD is also known to be an independent predictor of abdominal aortic aneurysm (AAA) growth and rupture. The purpose of this study is to determine the effect of

The Effect of Nicotine and Tobacco on Aortic Matrix Metalloproteinases in the Production of Aortic Aneurysm.

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Aortic aneurysms (AAs) are without effective pharmacologic therapy, in clinical usage, in part because of the limited understanding of factors leading to AA development. The objectives of this study were to examine the evidence that cigarette smoking induces AAs through altering matrix

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm

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Aim: Smoking is a major risk factor for abdominal aortic aneurysm (AAA). Among the components of smoke, nicotine is known to exert pro-atherosclerotic, prothrombotic, and proangiogenic effects on vascular smooth muscle cells (VSMCs). The current study was designed to investigate the

Tobacco smoking and aortic aneurysm: two population-based studies.

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BACKGROUND We determined the predictive power of tobacco smoking on aortic aneurysm as opposed to other risk factors in the general population. METHODS We recorded tobacco smoking and other risk factors at baseline, and assessed hospitalization and death from aortic aneurysm in 15,072 individuals

Chronic Nicotine Exposure Induces Murine Aortic Remodeling and Stiffness Segmentation-Implications for Abdominal Aortic Aneurysm Susceptibility.

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Aim: Arterial stiffness is a significant risk factor for many cardiovascular diseases, including abdominal aortic aneurysms (AAA). Nicotine, the major active ingredient of e-cigarettes and tobacco smoke, induces acute vasomotor effects that may temporarily increase arterial stiffness. Here, we

SP600125 Attenuates Nicotine-Related Aortic Aneurysm Formation by Inhibiting Matrix Metalloproteinase Production and CC Chemokine-Mediated Macrophage Migration.

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Nicotine, a major chemical component of cigarettes, plays a pivotal role in the development of abdominal aortic aneurysm (AAA). c-Jun N-terminal kinase (JNK) has been demonstrated to participate in elastase-induced AAA. This study aimed to elucidate whether the JNK inhibitor SP600125 can attenuate

MicroRNA-21 blocks abdominal aortic aneurysm development and nicotine-augmented expansion.

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Identification and treatment of abdominal aortic aneurysm (AAA) remains among the most prominent challenges in vascular medicine. MicroRNAs are crucial regulators of cardiovascular pathology and represent possible targets for the inhibition of AAA expansion. We identified microRNA-21 (miR-21) as a

Pathogenesis of abdominal aortic aneurysms: role of nicotine and nicotinic acetylcholine receptors.

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Inflammation, proteolysis, smooth muscle cell apoptosis, and angiogenesis have been implicated in the pathogenesis of abdominal aortic aneurysms (AAAs), although the well-defined initiating mechanism is not fully understood. Matrix metalloproteinases (MMPs) such as MMP-2 and -9 and other proteinases

Activation of AMP-activated protein kinase α2 by nicotine instigates formation of abdominal aortic aneurysms in mice in vivo.

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Smoking is the only modifiable risk factor that is associated with the development, expansion and rupture of abdominal aortic aneurysm (AAA). However, the causative link between cigarette smoke and AAA is unknown. Here we report a causative link between smoking and AAA in vivo. Acute infusion of

Tobacco smoking and the risk of abdominal aortic aneurysm: a systematic review and meta-analysis of prospective studies.

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Several studies have found that smoking increases the risk of abdominal aortic aneurysm, however, the strength of the association has differed between studies and data from cohort studies have not yet been summarized. A systematic review and meta-analysis was therefore conducted to clarify this

Understanding the effects of tobacco smoke on the pathogenesis of aortic aneurysm.

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Aneurysmal arterial disease is a vascular degenerative condition that is distinct from atherosclerotic and other occlusive arterial diseases. There is regionalization of the predisposition to aneurysm formation within the vascular tree, and the pathological process varies with location. Infrarenal

The development of abdominal aortic aneurysms in mice is enhanced by benzo(a)pyrene.

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Cigarette smoking has been strongly associated with abdominal aortic aneurysm (AAA), but the components of tobacco smoke involved in AAA have not been identified. Benzo(a)pyrene (BaP) is an important constituent in cigarette smoke capable of induction of alterations strikingly similar to the

The Seed Coat Extract of Black Soybean Decreases Nicotine-Induced Vascular Fiber Degradation by Suppressing Matrix Metalloproteinase 2 Expression.

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Logi sisse

Abdominal aortic aneurysm (AAA) is a vascular disease characterized by weakening of vascular walls and progressive dilation of the abdominal aorta. Nicotine, the main component of tobacco, is reportedly associated with the development and rupture of AAA. It is desirable to attenuate the destructive

Stimulation of Alpha7 Nicotinic Acetylcholine Receptor Attenuates Nicotine-Induced Upregulation of MMP, MCP-1, and RANTES through Modulating ERK1/2/AP-1 Signaling Pathway in RAW264.7 and MOVAS Cells.

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Vagus nerve stimulation through alpha7 nicotine acetylcholine receptors (α7-nAChR) signaling had been demonstrated attenuation of inflammation. This study aimed to determine whether PNU-282987, a selective α7-nAChR agonist, affected activities of matrix metalloproteinase (MMP) and inflammatory

Suppressive effects of dietary EPA-rich fish oil on the degradation of elastin fibers in the aortic wall in nicotine-administered mice.

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Abdominal aortic aneurysm (AAA) is a vascular disease involving gradual dilation of the abdominal aorta. Recent studies suggest that nicotine, which is a primary component in cigarette smoke, is closely associated with the development and rupture of an AAA. Nicotine accelerates AAA development

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