Adverse cardiac remodeling following myocardial infarction (MI) remains a significant cause
of congestive heart failure. Additional and novel strategies that improve our ability to predict …

Abstract Matrix metalloproteinase-9 (MMP-9) is robustly elevated in the first week post-
myocardial infarction (MI). Targeted deletion of the MMP-9 gene attenuates cardiac …

Matrix metalloproteinase (MMP)-9, one of the most widely investigated MMPs, regulates
pathological remodeling processes that involve inflammation and fibrosis in cardiovascular …

Over the past three decades, numerous studies have shown a strong connection between
matrix metalloproteinase 9 (MMP-9) levels and myocardial infarction (MI) mortality and left …

Matrix metalloproteinases (MMPs) and their endogenous inhibitors have been studied in the
myocardium for the past 2 decades. An incomplete knowledge base and experimental …

Despite current optimal therapeutic regimens, approximately one in four patients diagnosed
with myocardial infarction (MI) will go on to develop congestive heart failure, and heart …

Rationale: Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular
matrix responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI) …

Abstract Rationale Matrix metalloproteinases (MMPs) regulate remodeling of the left
ventricle (LV) post-myocardial infarction (MI). MMP-12 has potent macrophage-dependent …

Abstract Matrix metalloproteinase‐9 (MMP‐9) deletion has been shown to improve
remodeling of the left ventricle post‐myocardial infarction (MI), but the mechanisms to …

Matrix metalloproteinase-2 (MMP-2) is prominently overexpressed both after myocardial
infarction (MI) and in heart failure. However, its pathophysiological significance in these …