The balance between MMP-9 and endogenous inhibitor, tissue inhibitors of matrix metalloproteinase 1 (TIMP-1), is important in acute coronary syndrome (ACS).
To investigate whether focal adhesion kinase (FAK) can participate in the secretion of matrix metalloproteinase 9 (MMP9) after CD147 stimulation in THP-1 induced macrophages; thus, to explore the potential treatment perspectives for acute coronary syndrome (ACS).Phorbol-12-myristate-13-acetate (PMA) was used to induce THP-1 cells to differentiate into macrophages.
Pentraxin 3, long expression in mononuclear cells of patients with acute coronary syndrome: Correlation with C-reactive protein and matrix metalloproteinase-9 levels.
The obtained results permit to conclude that the increased expression of MMP-2 and MMP-9 metalloproteinases and their tissue inhibitor (TIMP-2) is responsible for disturbed equilibrium of the metalloproteinase/tissue inhibitors system and as a consequence, for destabilization of atherosclerotic plaque and occurrence of the acute coronary syndrome in the investigated group of patients.
Within this context, our aim was to examine whether MMP1, MMP3, and MMP9 gene polymorphisms are associated with susceptibility to acute coronary syndrome (ACS) or angiographic coronary artery disease (CAD).
Expression of toll-like receptor 4, tumor necrosis factor- alpha, matrix metalloproteinase-9 and effects of benazepril in patients with acute coronary syndromes.
The T allele of the PPARgamma gene might have a protective effect on the progression of CAD and reduce the onset of acute coronary syndrome, which might be associated with the decreased expression of MMP-9 and TNF-alpha in patients with CAD.
The present findings suggest that the genetic polymorphism in MMP-9 promoter (C-1562-T) is associated with the susceptibility to ACS in the Han population of China.