2008
DOI: 10.1016/j.atherosclerosis.2007.05.013
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Relation between interleukin-6 level and subclinical intracranial large-artery atherosclerosis

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Cited by 28 publications
(19 citation statements)
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“…52 Atherosclerosis lesion formation in different vascular beds may share common etiologic mechanisms. Increased levels of IL6 have been recently associated with intracranial large vessel atherosclerosis, 53 raising the possibility that the role of IL6 in atherogenesis may be similar in small and large vessels. IL6 is the principal regulator of acute-phase proteins and, therefore, plays a major role in the activation of the coagulation-fibrinolysis system.…”
Section: Discussionmentioning
confidence: 99%
“…52 Atherosclerosis lesion formation in different vascular beds may share common etiologic mechanisms. Increased levels of IL6 have been recently associated with intracranial large vessel atherosclerosis, 53 raising the possibility that the role of IL6 in atherogenesis may be similar in small and large vessels. IL6 is the principal regulator of acute-phase proteins and, therefore, plays a major role in the activation of the coagulation-fibrinolysis system.…”
Section: Discussionmentioning
confidence: 99%
“…5 In particular, the levels of circulating inflammatory markers, such as high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), and interleukin-18 (IL-18), could predict future risk of stroke and cardiovascular events. 6 -8 Several studies have demonstrated the association of inflammatory markers with the severity of vessel lesions in the carotid and intracranial arteries, 9,10 as well as with silent lacunar infarction (SLI) and white matter hyperintensities (WMH), 11,12 suggesting the involvement of inflammatory processes in SVD. Although a relationship between hsCRP, matrix metalloproteinase-9, and CMB was examined in acute stroke patients, 13 the relationship between CMB and inflammatory marker levels has not been investigated in individuals without a history of stroke.…”
mentioning
confidence: 99%
“…26 During the past 2 decades, increasing evidence has linked variations in the expression of inflammatory mediators, such as interleukin (IL)-6, IL-10, and 5-lipoxygenase, to stroke. [27][28][29][30][31][32] Atopic respiratory conditions have also been linked to similar changes in IL-6, IL-10, and 5-lipoxygenase. [33][34][35][36] Given these relationships, inflammation may be a critical link between atopic respiratory conditions and stroke.…”
Section: Discussionmentioning
confidence: 98%