How much is too much? Interleukin-6 and its signalling in atherosclerosis. Export

@article{citeulike:5976111, abstract = {The importance of inflammation as a driver of pathology is no longer confined to autoimmune and infectious diseases. In line with convincing experimental data as well as abundant clinical findings the current view of atherosclerosis points to inflammation as a critical regulator of atherosclerotic plaque formation and progression leading to the fatal clinical endpoints myocardial infarction, stroke or sudden cardiac death. The underlying mechanisms have been a matter of intense research during the last decades. In this regard, the interleukin-6 (IL-6) cytokines and their signalling events have been shown to contribute to both, atherosclerotic plaque development and plaque destabilisation via a variety of mechanisms. These involve the release of other pro-inflammatory cytokines, oxidation of lipoproteins by phospholipases, stimulation of acute phase protein secretion, the release of prothrombotic mediators, and the activation of matrix metalloproteinases. Moreover, the formation of reactive oxygen species generated by vascular enzyme systems may play a critical role in the regulation of IL-6 indicating a cross talk between vasoactive substances i.e. angiotensin II or adrenalin and pro-inflammatory cytokines such as IL-6. In this review we will summarise and discuss the underlying molecular and cellular mechanisms how IL-6 as an early and central regulator of inflammation contributes to atherosclerosis and how this knowledge can be integrated into the clinical context.}, author = {Schuett, Harald and Luchtefeld, Maren and Grothusen, Christina and Grote, Karsten and Schieffer, Bernhard}, citeulike-article-id = {5976111}, citeulike-linkout-0 = {http://dx.doi.org/10.1160/TH09-05-0297}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19652871}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19652871}, citeulike-linkout-3 = {http://scholar.google.com/scholar?cluster=16672638726516382774}, doi = {10.1160/TH09-05-0297}, issn = {0340-6245}, journal = {Thrombosis and haemostasis}, keywords = {atherosclerosis, cvd, epc, il6, il6-n-angio, revu}, month = {August}, number = {2}, pages = {215--222}, posted-at = {2009-10-20 19:47:19}, priority = {2}, title = {How much is too much? Interleukin-6 and its signalling in atherosclerosis.}, url = {http://dx.doi.org/10.1160/TH09-05-0297}, volume = {102}, year = {2009} }

TY - JOUR ID - citeulike:5976111 L3 - citeulike-article-id:5976111 N2 - The importance of inflammation as a driver of pathology is no longer confined to autoimmune and infectious diseases. In line with convincing experimental data as well as abundant clinical findings the current view of atherosclerosis points to inflammation as a critical regulator of atherosclerotic plaque formation and progression leading to the fatal clinical endpoints myocardial infarction, stroke or sudden cardiac death. The underlying mechanisms have been a matter of intense research during the last decades. In this regard, the interleukin-6 (IL-6) cytokines and their signalling events have been shown to contribute to both, atherosclerotic plaque development and plaque destabilisation via a variety of mechanisms. These involve the release of other pro-inflammatory cytokines, oxidation of lipoproteins by phospholipases, stimulation of acute phase protein secretion, the release of prothrombotic mediators, and the activation of matrix metalloproteinases. Moreover, the formation of reactive oxygen species generated by vascular enzyme systems may play a critical role in the regulation of IL-6 indicating a cross talk between vasoactive substances i.e. angiotensin II or adrenalin and pro-inflammatory cytokines such as IL-6. In this review we will summarise and discuss the underlying molecular and cellular mechanisms how IL-6 as an early and central regulator of inflammation contributes to atherosclerosis and how this knowledge can be integrated into the clinical context. IS - 2 JF - Thrombosis and haemostasis SN - 0340-6245 EP - 222 TI - How much is too much? Interleukin-6 and its signalling in atherosclerosis. VL - 102 SP - 215 KW - atherosclerosis KW - cvd KW - epc KW - il6 KW - il6-n-angio KW - revu AU - Schuett, Harald AU - Luchtefeld, Maren AU - Grothusen, Christina AU - Grote, Karsten AU - Schieffer, Bernhard PY - 2009/08// UR - http://dx.doi.org/10.1160/TH09-05-0297 ER -