Immunohistochemical Features of Different Types of Unstable Atherosclerotic Plaques of Coronary Arteries

Early identification of carotid vulnerable plaque in asymptomatic patients

“…The weakening of the fibrous cap due to the net degradation of the extracellular matrix is considered to be an important cause of plaque rupture. MMP-9, also known as gelatinase B [15,16], is highly expressed in macrophage-rich atheromatous plaque regions, and its main function is to mediate the degradation and remodeling of ECM, as well as the degradation of all components of the vascular wall, so it plays an important role in the degradation of the fibrous cap in arterial plaque. Laura [17] found that MMP-9 can promote the transformation of plaque from stable to vulnerable state, increase plaque instability, and MMP-9 has certain value for the prediction, diagnosis and prognosis of acute coronary syndrome.…”

Discoidin domain-containing receptor 2 is present in human atherosclerotic plaques and involved in the expression and activity of MMP-2

“…Notably, given that this depends on the secretion of MMPs, another question has been raised as to whether DDR2 also regulates MMPs (28). Indeed, MMPs can almost determine the fate of atherosclerotic plaques because MMP-mediated breakdown of ECM is a typical feature of an unstable plaque (29). In pathological conditions, excessive ECM also stimulates VSMCs to degrade ECM as a negative feedback regulation.…”

An Exonic Switch Regulates Differential Accession of microRNAs to the Cd34 Transcript in Atherosclerosis Progression

“…Originally characterized as an hemopoietic progenitor cell marker [40], CD34 was subsequently detected in vascular endothelial cells [41] and neovascularized tissues [42]. CD34 has been shown to be important in the development of ATH lesions, mainly in neo/re-vascularization events, with CD34-positive cells being detected more frequently in inflammatory-erosive plaques, when compared with plaques of the lipid or degenerative-necrotic plaques [43]. It is thus evident that elucidating the mechanisms of CD34 expression and CD34-cell differentiation would have a positive impact on CVD disease.…”