The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?

Atherogenesis is characterized by an intense inflammatory process, involving immune and vascular cells. These cells play a crucial role in all phases of atherosclerotic plaque formation and complication through cytokine, protease, and prothrombotic factor secretion. The accumulation of inflammatory...

Full description

Saved in:
Bibliographic Details
Main Authors: Fabrizio Montecucco, Sabine Steffens, François Mach
Format: Article
Language:English
Published: Wiley 2007-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2007/75805
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832558298441711616
author Fabrizio Montecucco
Sabine Steffens
François Mach
author_facet Fabrizio Montecucco
Sabine Steffens
François Mach
author_sort Fabrizio Montecucco
collection DOAJ
description Atherogenesis is characterized by an intense inflammatory process, involving immune and vascular cells. These cells play a crucial role in all phases of atherosclerotic plaque formation and complication through cytokine, protease, and prothrombotic factor secretion. The accumulation of inflammatory cells and thus high amounts of soluble mediators are responsible for the evolution of some plaques to instable phenotype which may lead to rupture. One condition strongly associated with plaque rupture is calcification, a physiopathological process orchestrated by several soluble factors, including the receptor activator of nuclear factor NFκB ligand (RANKL)/receptor activator of nuclear factor NFκB (RANK)/osteoprotegerin (OPG) system. Although some studies showed some interesting correlations with acute ischemic events, at present, more evidences are needed to evaluate the predictive and diagnostic value of serum sRANKL and OPG levels for clinical use. The major limitation is probably the poor specificity of these factors for cardiovascular disease. The identification of tissue-specific isoforms could increase the importance of sRANKL and OPG in predicting calcified plaque rupture and the dramatic ischemic consequences in the brain and the heart.
format Article
id doaj-art-1e3b7280afd843a08ce93fcf9b504561
institution Kabale University
issn 1740-2522
1740-2530
language English
publishDate 2007-01-01
publisher Wiley
record_format Article
series Clinical and Developmental Immunology
spelling doaj-art-1e3b7280afd843a08ce93fcf9b5045612025-02-03T01:32:36ZengWileyClinical and Developmental Immunology1740-25221740-25302007-01-01200710.1155/2007/7580575805The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?Fabrizio Montecucco0Sabine Steffens1François Mach2Division of Cardiology, Foundation for Medical Researches, University Hospital of Geneva, Geneva 1211, SwitzerlandDivision of Cardiology, Foundation for Medical Researches, University Hospital of Geneva, Geneva 1211, SwitzerlandDivision of Cardiology, Foundation for Medical Researches, University Hospital of Geneva, Geneva 1211, SwitzerlandAtherogenesis is characterized by an intense inflammatory process, involving immune and vascular cells. These cells play a crucial role in all phases of atherosclerotic plaque formation and complication through cytokine, protease, and prothrombotic factor secretion. The accumulation of inflammatory cells and thus high amounts of soluble mediators are responsible for the evolution of some plaques to instable phenotype which may lead to rupture. One condition strongly associated with plaque rupture is calcification, a physiopathological process orchestrated by several soluble factors, including the receptor activator of nuclear factor NFκB ligand (RANKL)/receptor activator of nuclear factor NFκB (RANK)/osteoprotegerin (OPG) system. Although some studies showed some interesting correlations with acute ischemic events, at present, more evidences are needed to evaluate the predictive and diagnostic value of serum sRANKL and OPG levels for clinical use. The major limitation is probably the poor specificity of these factors for cardiovascular disease. The identification of tissue-specific isoforms could increase the importance of sRANKL and OPG in predicting calcified plaque rupture and the dramatic ischemic consequences in the brain and the heart.http://dx.doi.org/10.1155/2007/75805
spellingShingle Fabrizio Montecucco
Sabine Steffens
François Mach
The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
Clinical and Developmental Immunology
title The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
title_full The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
title_fullStr The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
title_full_unstemmed The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
title_short The Immune Response Is Involved in Atherosclerotic Plaque Calcification: Could the RANKL/RANK/OPG System Be a Marker of Plaque Instability?
title_sort immune response is involved in atherosclerotic plaque calcification could the rankl rank opg system be a marker of plaque instability
url http://dx.doi.org/10.1155/2007/75805
work_keys_str_mv AT fabriziomontecucco theimmuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability
AT sabinesteffens theimmuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability
AT francoismach theimmuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability
AT fabriziomontecucco immuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability
AT sabinesteffens immuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability
AT francoismach immuneresponseisinvolvedinatheroscleroticplaquecalcificationcouldtheranklrankopgsystembeamarkerofplaqueinstability