Inflammation in Atherosclerosis

Lucas, Alexandra; Korol, Renée; Pepine, Carl J.

doi:10.1161/circulationaha.105.601492

Cited by 55 publications

(18 citation statements)

References 25 publications

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“…Likewise, all-cause hospitalisations can be markers of poor general health and, hence, poor prognosis. Other more specific factors may also operate in particular causes of admissions including: 1) a burst of systemic inflammation, known to occur during exacerbations of COPD [24] or acute cardiovascular diseases [25], that can reduce quadriceps strength and exercise capacity [12]; or 2) the use of systemic corticosteroid therapy [1,18], commonly used in case of COPD admissions, that can cause skeletal muscle dysfunction [26]. The fact that, in this study, neither the total duration of hospital stay nor the time from hospital discharge to the second evaluation were related to the annual 6MWD decline suggest that other specific mechanisms may play a more active and important pathogenic role than simply the passive physical inactivity associated with any hospitalisation event.…”

Section: Interpretation Of Findingsmentioning

confidence: 99%

Hospital admissions and exercise capacity decline in patients with COPD

et al. 2014

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Exercise capacity declines with time and is an important determinant of health status and prognosis in patients with chronic obstructive pulmonary disease (COPD). We hypothesised that hospital admissions are associated with exercise capacity decline in these patients.Clinical and functional variables were collected for 342 clinically stable COPD patients. The 6-min walk distance (6MWD) was determined at baseline and after a mean¡SD of 1.7¡0.3 years. Information on hospitalisations during follow-up was obtained from centralised administrative databases. Linear regression was used to model changes in exercise capacity.Patients were mostly male (92%), with mean¡SD age 67.9¡8.6 years, post-bronchodilator forced expiratory volume in 1 s 54¡17% predicted and baseline 6MWD 433¡93 m. During follow-up, 6MWD decreased by 21.9¡51.0 m?year -1 and 153 (45%) patients were hospitalised at least once. Among patients admitted only for COPD-related causes (50% of those ever admitted), the proportion presenting a clinically significant loss of 6MWD was higher than in patients admitted for only nonrespiratory conditions (53% versus 29%, p50.040). After adjusting for confounders, annual 6MWD decline was greater (26 m?year -1 , 95% CI 13-38 m?year -1 ; p,0.001) in patients with more than one all-cause hospitalisation per year, as compared with those with no hospitalisations.Hospitalisations are related to a greater decline in exercise capacity in COPD.@ERSpublications Hospitalisations are associated with higher decline in exercise capacity in COPD patients

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Section: Interpretation Of Findingsmentioning

confidence: 99%

Hospital admissions and exercise capacity decline in patients with COPD

et al. 2014

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“…Atherosclerosis is now recognized as a chronic inflammatory process since inflammation is involved in all stages of atherosclerosis from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis [38,[90][91][92]. Vascular endothelium, which not only serves as a biological barrier separating circulating blood and peripheral tissues, but also secretes various vasoactive substances, plays a pivotal role in maintaining normal vascular function.…”

Section: Genistein and Vascular Inflammationmentioning

confidence: 99%

Phytochemical Genistein in the Regulation of Vascular Function: New Insights

Liu²

2007

CMC

105

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Genistein, a natural bioactive compound derived from legumes, has drawn wide attention during the last decade because of its potentially beneficial effects on some human degenerative diseases. It has a weak estrogenic effect and is a well-known non-specific tyrosine kinase inhibitor at pharmacological doses. Epidemiological studies show that genistein intake is inversely associated with the risk of cardiovascular diseases. Data from animal and in vitro studies suggest a protective role of genistein in cardiovascular events. However, the mechanisms of the genistein action on vascular protective effects are unclear. Past extensive studies exploring its hypolipidemic effect resulted in contradictory data. Genistein also is a relatively poor antioxidant. However, genistein protects against pro-inflammatory factor-induced vascular endothelial barrier dysfunction and inhibits leukocyte-endothelium interaction, thereby modulating vascular inflammation, a major event in the pathogenesis of atherosclerosis. Recent studies found that genistein exerts a novel non-genomic action by targeting on important signaling molecules in vascular endothelial cells (ECs). Genistein rapidly activates endothelial nitric oxide synthase and production of nitric oxide in ECs. This genistein effect is novel since it is independent of its known effects, but mediated by the cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) cascade. Further studies demonstrated that genistein directly stimulates the plasma membrane-associated adenylate cyclases, leading to activation of the cAMP signaling pathway. In addition, genistein activates peroxisome proliferator-activated receptors, ligand-activated nuclear receptors important to normal vascular function. Furthermore, genistein reduces reactive oxygen species (ROS) by attenuating the expression of ROS-producing enzymes. These new findings reveal the novel roles for genistein in the regulation of vascular function and provide a basis for further investigating its therapeutic potential for inflammatory-related vascular disease.

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“…The fact that inflammation has a pivotal role in the development of atherosclerosis has intensified the search for chronic exposure to infectious organisms that have the potential to cause inflammation in vessels (Libby et al, 2002;Lucas et al, 2006). One type of atherosclerosis, restenosis, results from rapid plaque growth after percutaneous intervention with balloon angioplasty (BA) (Jones et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Increased Atherogenesis during Streptococcus mutans Infection in ApoE-null Mice

et al. 2012

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A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental. AbstrAct Streptococcus mutans, a dental caries pathogen, also causes endocarditis and is detected in atheroscelerotic plaque. We investigated the potential for an invasive strain of S. mutans, OMZ175, to accelerate plaque growth in apolipoprotein E deficient (ApoE null ) mice without and with balloon angioplasty (BA) injury, a model of restenosis. ApoE null mice were divided into 4 groups (N = 10), 2 with and 2 without BA. One each of the BA and non-BA groups was infected with S. mutans (Sm). S. mutans DNA, plaque area, inflammatory cell invasion, and Toll-like receptor (TLR) expression were measured at 6-20 weeks post-infection. S. mutans genomic DNA was detected in the aorta, liver, spleen, and heart. Plaque growth was significantly increased in infected mice with BA (Sm+BA) vs. those in the non-infected groups (p < 0.03). Plaque size was increased after infection without BA (Sm), but did not reach significance. Aortic specimens from both S. mutans and Sm+BA groups displayed increased numbers of macrophages, and TLR4 expression was increased in BA mice. In conclusion, S. mutans infection accelerated plaque growth, macrophage invasion, and TLR4 expression after angioplasty. S. mutans may also be associated with atherosclerotic plaque growth in non-injured arteries.

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Inflammation in Atherosclerosis

Cited by 55 publications

References 25 publications

Hospital admissions and exercise capacity decline in patients with COPD

Hospital admissions and exercise capacity decline in patients with COPD

Phytochemical Genistein in the Regulation of Vascular Function: New Insights

Increased Atherogenesis during Streptococcus mutans Infection in ApoE-null Mice

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