Angiotensin II and Atherosclerosis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2004

AUTHORS

H. Drexler , B. Schieffer

ABSTRACT

Atherosclerosis is a chronic inflammatory disease perpetuated by a variety of pro-inflammatory mediators. Fatal endpoints of this inflammatory disease are myocardial infarction, stroke or sudden death, which together remain the major cause of morbidity and mortality in industrialized countries. Accumulated evidence obtained from pathological observations, state-of-the-art imaging and large-scale clinical trials showed that these fatal events are mainly endpoints of pathological vascular remodeling processes, suggesting a close interaction between inflammation and vascular remodeling. In this regard, the renin- angiotensin system (RAS) was—at least partially—accused of contributing to the development and/or progression of atherosclerosis. The Heart Outcome and Prevention Evaluation (HOPE) study convincingly demonstrated that clinical blockade of the RAS may reduce fatal endpoints of severe atherosclerosis, which is characterized by the pathological triad of inflammation, RAS and remodeling: this suggests a role for the RAS in plaque development and stability. Since experimental and clinical evidence point to inflammatory mediators such as interferon-γ, interleukin-1β, interleukin-18 and -10, and interleukin-6 (1) as promotors/predictors of cardiovascular events, we will discuss the clinical basis and the potential molecular and cellular interactions between the RAS and cytokines, and their potential impact on remodeling processes at the atherosclerotic plaques. In particular, we will focus on the interaction of angiotensin II (ANG II) and cytokines such as interleukin 6 (IL-6), and their potential impact on plaque development and stability More... »

PAGES

21-38

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-18497-0_2

DOI

http://dx.doi.org/10.1007/978-3-642-18497-0_2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1002766488


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