Matrix metalloproteinases in pro-atherosclerotic arterial remodeling

Glycosylation is important for legumain localization and processing to active forms but not for cystatin E/M inhibitory functions

“…The authors postulated that legumain represents a novel target for treatment of unstable plaques or as a diagnostic marker of plaque instability. Also, degradation of ECM caused by proteolytic enzymes is an important factor in destabilization of atherosclerotic plaques, as shown for MMPs (recently reviewed in [292,293]). In addition to activation of MMP-2, legumain can directly degrade fibronectin, a major component of ECM [73,108].…”

Matrix Metalloproteinases as Biomarkers of Atherosclerotic Plaque Instability

“…[6]. MMPs play important role in maintaining vein wall structure and function, but on the other hand, in adverse cardiovascular remodeling, atherosclerotic plaque formation and plaque instability [7,8]. Serum elevation of MMP-2, ADAMTS-1, and ADAMTS-7 is correlated with the initial stages of chronic venous disease (CVD), whereas the serum elevation of MMP-1, MMP-8, MMP-9, NGAL, ADAM-10, ADAM-17, and ADAMTS-4 is particularly involved in skin change complications [9].…”

Association between serum HER2/ErbB2 levels and coronary artery disease: a case–control study

“…Meanwhile, the HER2 shedding process, which is attributed to various zinc-containing metalloproteases, including matrix metallo-protease (MMP) families, can increase the tyrosine kinase activity and amplify HER2 signaling [5]. MMP families are well known to degrade structural proteins of the extracellular matrix, for example, the collagenous matrix in the fibrous cap and adjacent shoulder regions, and play critical roles in the instability of plaques [24]. Intriguingly, enhanced HER2 signaling can, in turn, promote the transcription of MMP families, thus probably creating a vicious cycle in the setting of atherosclerosis [25].…”