CD163
atherosclerosis
cell adhesion molecules
collagen
coronary stenosis
macrophages
Journal
Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103
Informations de publication
Date de publication:
11 Jun 2024
11 Jun 2024
Historique:
medline:
11
6
2024
pubmed:
11
6
2024
entrez:
11
6
2024
Statut:
aheadofprint
Résumé
Cell phenotype switching is increasingly being recognized in atherosclerosis. However, our understanding of the exact stimuli for such cellular transformations and their significance for human atherosclerosis is still evolving. Intraplaque hemorrhage is thought to be a major contributor to plaque progression in part by stimulating the influx of CD163 Human coronary artery sections from CVPath's autopsy registry were selected for pathological analysis. Athero-prone In 107 lesions with acute coronary plaque rupture, 55% had pathological evidence of intraplaque hemorrhage in nonculprit vessels/lesions. Thinner fibrous cap, greater CD163 CD163
Sections du résumé
BACKGROUND
UNASSIGNED
Cell phenotype switching is increasingly being recognized in atherosclerosis. However, our understanding of the exact stimuli for such cellular transformations and their significance for human atherosclerosis is still evolving. Intraplaque hemorrhage is thought to be a major contributor to plaque progression in part by stimulating the influx of CD163
METHODS
UNASSIGNED
Human coronary artery sections from CVPath's autopsy registry were selected for pathological analysis. Athero-prone
RESULTS
UNASSIGNED
In 107 lesions with acute coronary plaque rupture, 55% had pathological evidence of intraplaque hemorrhage in nonculprit vessels/lesions. Thinner fibrous cap, greater CD163
CONCLUSIONS
UNASSIGNED
CD163
Identifiants
pubmed: 38860377
doi: 10.1161/CIRCRESAHA.123.324082
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM