MMP-2 and TIMP-2 in patients with heart failure and chronic kidney disease

Abstract

<jats:title>Abstract</jats:title><jats:p>The aim of the study was to assess MMP-2 (matrix metalloproteinase-2) and TIMP-2 (tissue inhibitor of metalloproteinase-2) serum levels in patients with diverse types of heart failure (HF) and chronic kidney disease (CKD).</jats:p><jats:p>101 patients with chronic HF were enrolled. Each patient has assessed the serum levels of MMP-2, TIMP-2, and NT-proBNP. Patients were initially classified into 2 groups based on their LVEF. 43 patients were classified into the HFREF group (HF with Reduced Ejection Fraction) and 58 characterized as HFPEF (HF with Preserved Ejection Fraction). Next, all patients were subdivided into 4 groups according to the degree of diastolic dysfunction.</jats:p><jats:p>38 patients with CKD were classified into HF/CKD(+) group. The HF/CKD(-) (HF without CKD) group comprised 61 patients.</jats:p><jats:p>This study provides original data on positive correlation between ejection fraction and MMP-2 levels in all patients with heart failure. Elevated levels of MMP-2 and TIMP-2 were found in serum from patients with chronic kidney disease; in addition, serum levels of MMP-2 were correlated with the degree of kidney failure. In all groups of patients there was positive correlation between MMP-2 and TIMP-2. Among patients with heart failure etiology was not related to MMP-2 and TIMP-2 serum levels.</jats:p>

Injectable Myocardial Matrix Hydrogel Mitigates Negative Left Ventricular Remodeling in a Chronic Myocardial Infarction Model

“…Interestingly, in this study we demonstrated an alternate modulation of the inflammatory and immune response. In matrix-treated animals there was reduced expression of Mmp2 and Timp2, which are both associated with chronic inflammation in HF leading to fibrosis, increased wall stiffness, and reduced contractility (36). While the in vitro data suggests the matrix is able to promote MMP-2 production (Figure 4), this assay only assessed cardiac fibroblast MMP production and the in vivo gene expression analysis takes into account all cell types located in the infarct region of the myocardium such as immune cells, which are known to produce MMPs (28).…”

“…(29,35). Additionally, we showed downregulation of matrix metalloproteinase 2 (Mmp2) and tissue inhibitor of Mmp2 (Timp2), both of which are associated with fibrogenesis in HF (Figure 5)(25,36), as well as downregulation of matrix metalloproteinase 2 (Mmp2) and tissue inhibitor of Mmp2 (Timp2), both of which are associated with fibrogenesis in HF (Figure 5). We also observed downregulation of Tlr2, Fos, Akt3, Fcer1a, CD68, Cxcl11, and Pf4 and upregulation of Ccl11 showing modulation of the immune response towards an anti-inflammatory response (Figure 5)(32).…”

Novel heart failure biomarkers: why do we fail to exploit their potential?

“…Also, in humans, inhibition of IL-6 has been tested, but it was not able to improve coronary flow reserve in patients post-myocardial infarction [114]. Nevertheless, because IL-6 has been shown to be involved in HF development, and because levels of this inflammatory marker are increased in HF and are able to predict HF outcome in various types of HF [5,[115][116][117][118][119], it could serve as an HF biomarker. The use of IL-6 in a multi-biomarker model has been suggested [120], but circulating IL-6 levels are also affected by factors like stress, physical exercise, gender and age [119].…”

Yixinshu ameliorates hippocampus abnormality induced by heart failureviathe PPARγ signaling pathway

“…27 In this study, inammatory cytokines, such as TNF-alpha, in the serum increased, consistent with the results previously reported. 20,28 Moreover, YXS can increase the expression of ZO-1 and AQP4, which implies that YXS had a protective effect in maintaining the integrity of the BBB. On the other hand, YXS can signicantly decrease the levels of IL1-beta, IL-6 and TNF-alpha in the hippocampus in rats with HF compared to the model group.…”