Mechanisms Underlying Atheroma Induction: The Roles of Mechanotransduction, Vascular Wall Cells, and Blood Cells

The objective of this article is to review cellular mechanism of atherosclerosis (AS) development. The pathogenesis of AS comprises a sequence of biological events leading to build up of a dense or loose atheromatous plaque (AP). In this review, we tried to attempt to analyze the cellular mechanisms...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Annals of vascular surgery 2018-11, Vol.53, p.224-233
Hauptverfasser: Novikova, Olga A., Laktionov, Pavel P., Karpenko, Andrey A.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The objective of this article is to review cellular mechanism of atherosclerosis (AS) development. The pathogenesis of AS comprises a sequence of biological events leading to build up of a dense or loose atheromatous plaque (AP). In this review, we tried to attempt to analyze the cellular mechanisms underlying AS development, including the roles of monocytes/macrophages and smooth muscle cells in the formation of stable/unstable APs. As a rule, APs are formed in the regions with irregular blood flow; both mechanical perturbations of the vascular wall and several biological events contribute to plaque formation. Blood lipid/lipoprotein deposition, recruitment of monocytes/macrophages, foam cell formation, migration and proliferation of smooth muscle cells, secretion of extracellular matrix, and formation of the connective tissue in plaques are among the latter events. The review briefs the contributions of different processes to atheroma formation and describes the molecular mechanisms involved in AS development. AP transcriptome studies will be helpful in the identification of the key genes involved in atheroma transformation and development as well as discovery of the new targets for diagnosis and therapy.
ISSN:0890-5096
1615-5947
DOI:10.1016/j.avsg.2018.04.030