Thursday, September 19, 2019
Matrix Metalloproteinases Essay -- Biology, Science Experiments
Matrix metalloproteinases are members of a large family of enzymes that can degrade extracellular matrix as well as other molecules [1]. MMPs participate in a broad variety of normal and pathologic states [2], and have been implicated as potential mediators of cardiac dilation and heart failure. Indeed, in culture cells [3,4], animal models mimicking the CHF syndrome [5,6] and CHF patients [7-9], a mechanistic relationship has been demonstrated respect to myocardial MMP expression and left ventricular (LV) remodeling process [3-9]. Likewise, recent reports on endothelial culture cells [10-12] and animal models of CHF [13,14] have shown that the increase of expression and activity of MMP-2 and MMP-9 (called gelatinases) might also play an important role in the impairement of endothelial function, a key event contributing on morbidity and mortality in CHF patients [15]. However, data respect to the role of MMPs on endothelial dysfunction in the setting of human CHF is completely unknow n. Therefore, the aim of this study was to assess the association between the activity of gelatinases and endothelial dysfunction in patients with CHF. We hypothesized that a higher plasma MMP-2 and MMP-9 activities correlate with a lower endothelial function in patients with CHF. We included CHF patients, NYHA functional class II-III controlled in a university clinical center. All patients signed an informed consent approved by our institutional Review Board and Ethics Committee. Inclusion criteria were left ventricular ejection fraction (LVEF) ...esented here share new clinical evidence suggesting a possible participation of MMP-2 and MMP-9 in the genesis and progression of endothelial dysfunction, suggesting an active role of MMPs in this event. The main limitations of the present study were the limited number of patients, the presence of standard pharmacological therapy administered that may influence our results and such a correlations reported here did not demostrate a cause-effect relationship, but there is experimental evidence that could sustain our results. Further studies are clearly required to address this issue for exploring the causal relationships between these proteases and the pathophysiology of endothelial function. Acknowledgements The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [20].
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