Details

Autor(en) / Beteiligte

• SCHRIJVERS, Dorien M
• DE MEYER, Guido R. Y
• HERMAN, Arnold G
• MARTINET, Wim

Titel

Phagocytosis in atherosclerosis : Molecular mechanisms and implications for plaque progression and stability

Ist Teil von

• Cardiovascular research, 2007-02, Vol.73 (3), p.470-480

Ort / Verlag

Oxford: Oxford University Press

Erscheinungsjahr

2007

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• Macrophages play a key role in atherosclerotic plaque destabilization and rupture. In this light, selective removal of macrophages may be beneficial for plaque stability. However, macrophages are phagocytic cells and thus have an important additional role in scavenging of modified lipoproteins, unwanted or dead cells and cellular debris via phagocytosis. The concept of phagocytosis as well as the underlying mechanisms is well defined but the effect of phagocytosis in terms of plaque stability remains poorly understood. Recent findings point towards a complex role of macrophage phagocytosis in atherogenesis. Macrophages are necessary for removal of apoptotic cells from plaques, but exert strong proatherogenic properties upon phagocytosis of lipoproteins, erythrocytes and platelets. Apart from heterophagy, autophagocytosis better known as autophagy may occur in advanced atherosclerotic plaques. Several lines of evidence indicate that autophagy is initiated in plaque smooth muscle cells as a result of cellular distress. Since autophagy is well recognized as a survival mechanism, autophagic smooth muscle cells in the fibrous cap may reflect an important feature underlying plaque stability. All together, phagocytosis is a crucial process involved in atherogenesis that may significantly affect the stability of the atherosclerotic plaque.