PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9833074

[Current data on atheromatous plaques and their evolution].

C Bauters·E Van Belle·E McFadden·M Bertrand
View original source ↗Export metadata ↓

Abstract

The modes of evolution of atheromatous plaques are now better understood. The process may start very early and continue for several decades. The severity of atherosclerosis lies in the results of phases of rapid progression involving a thrombotic mechanism. An initial mechanical accident (rupture or erosion of the plaque) is followed by a phenomenon of arterial thrombosis of variable severity. The vulnerability of an atheromatous plaque (defined as its potential for acute complication) is related to: 1) the risk of rupture, 2) the risk of thrombosis in case of rupture. A number of intrinsic properties influence the degree of plaque vulnerability. A thorough understanding of these mechanisms is essential for the development of new treatments to improve the prognosis of coronary patients.

Explore related subjects

ArteriosclerosisCoronary Artery DiseaseCoronary DiseaseHumansEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C Bauters, E Van Belle, E McFadden, M Bertrand. 1998. [Current data on atheromatous plaques and their evolution].. https://pubmed.ncbi.nlm.nih.gov/9833074/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2002

Superoxide production and expression of nox family proteins in human atherosclerosis.

BACKGROUND: NAD(P)H oxidases are important sources of superoxide in the vasculature, the activity of which is associated with risk factors for human atherosclerosis. This study was designed to investigate the localization of superoxide production and the expression of the Nox family of NAD(P)H oxidase proteins (gp91phox, Nox1, and Nox4) in nonatherosclerotic and atherosclerotic human coronary arteries. METHODS AND RESULTS: In coronary artery segments from explanted human hearts, we examined intracellular superoxide production with dihydroethidium. In nonatherosclerotic coronary arteries, superoxide was present homogenously throughout the intima, media, and adventitia. In atherosclerotic arteries, there was an additional intense area of superoxide in the plaque shoulder, which is rich in macrophages and alpha-actin-positive cells. p22phox colocalized with gp91phox mainly in macrophages, whereas Nox4 was found only in nonphagocytic vascular cells. Expression of gp91phox and p22phox mRNA was associated with the severity of atherosclerosis. gp91phox correlated with the plaque macrophage content, whereas Nox4 correlated with the content of alpha-actin-positive cells. Nox1 expression was low both in human coronary arteries and isolated vascular cells. CONCLUSIONS: Several Nox proteins, including gp91phox and Nox4, may contribute to increased intracellular oxidative stress in human coronary atherosclerosis in a cell-specific manner and thus may be involved in the genesis and progression of human coronary atherosclerotic disease.

Arteriosclerosis↗