Renin-angiotensin system and coronary artery disease — Interaction of angiotensin II with pro-inflammatory cytokines in human stable and unstable coronary ... View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2000

AUTHORS

B. Schieffer , Helmut Drexler

ABSTRACT

Elevated inflammatory markers, such as cytokines (e.g., interleukin 6) and acute phase reactants (C-reactive protein and serum amyloid A) are one of the characteristics of patients with acute coronary syndromes (ACS). In addition, patients with genetically determined elevated serum levels of components of the renin angiotensin system (RAS) have a higher risk of myocardial infarction (MI). Inhibition of angiotensin II formation by angiotensin converting enzyme (ACE) inhibitors reduces the risk of re-infarction in patients after MI as shown in large scale clinical trials, such as SAVE, SOLVD, and AIRE.Angiotensin II, the effector peptide of the RAS activates via its G-protein coupled type 1 receptor (AT1) the cascade of Jak kinases and transcription factors of the STAT family (signal transducers and activators of transcription) which is traditionally involved in cytokine induction. In-vitro experiments demonstrated that an activated RAS, via the JAK/STAT cascade, interacts with proinflammatory cytokines, e.g., I1–6, which in turn induces the release of prothromobotic factors, such as plasminogen activator 1 and the synthesis of acute phase reactant C-RP and α2-macroglobulin. Blockade of the either the AT1 receptor or the tyrosine kinase JAK2 abolished this effect. Moreover, in-vivo findings obtained by immunhistochemistry in explanted human coronary arteries revealed that ACE, AII, AT1 receptor, and IL-6 are co-localized with macrophages (CD68 positive cells) at the shoulder region of the plaque. Similarly, co-localization of ACE, AII, AT1 receptor and I1–6 was documented in atherectomy samples obtained from patients with unstable angina and All was localized in close proximity to the presumed rupture site of human coronary arteries in acute MI. Thus, these results emphasize that the renin angiotensin system may contribute to inflammatory processes within the vascular wall and thereby may amplify the development of an acute coronary syndrome. More... »

PAGES

127-141

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-57724-6_11

DOI

http://dx.doi.org/10.1007/978-3-642-57724-6_11

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1002558401


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