The important role of plaque angiogenesis and subsequent plaque destabilization has been presented as this mechanism plays such an important role in plaque rupture and acute coronary syndromes.
Jander, S. et al. Expression of tissue factor in high-grade carotid artery stenosis: association with plaque destabilization.
The present study was designed to investigate whether Th3 cells are involved in plaque destabilization and the onset of ACS.
Oxidized LDL (OxLDL), a highly proinflammatory and proatherogenic factor that is abundant in atherosclerotic plaques, plays a pivotal role in plaque destabilization, which makes OxLDL a relevant probe target.
CD40 ligand (CD40L) is a trimeric, transmembrane protein of the tumor necrosis factor family and together with its receptor CD40 is an important contributor to the inflammatory processes that lead to atherosclerosis, plaque destabilization, and thrombosis.
The philosophy of prophylaxis and ways to improve patient compliance and achieve proper mechanical plaque removal are discussed.
Studies of macrophage polarization in vitro and in mostly mouse models of atherosclerosis have led to a simplified view that M1 macrophages are facilitating the formation of the necrotic core and plaque destabilization, whereas M2 macrophages have anti-atherogenic properties mediating plaque stability [22].
Likewise, in vascular smooth muscle cells (VSMCs) CTGF overexpression induced apoptosis [88] and led to MMP2 activity [89] which would result in plaque destabilization.
This clinical and pre- clinical data provides evidence supporting an important role for Cav-1, and its related peptides, in vascular pathologies such as intimal hyperplasia, expansive remodeling and human atherosclerotic plaque destabilization and rupture.
Moreover, activation of T cells is considered to play an important role in the process of atherosclerotic plaque destabilization which may initiate plaque disruption and the onset of acute coronary syndromes[5] [7] In general, the effector functions of activated T cells are under tight control of a special subset of T cells, the regulatory T cells (Treg).
