4.5 Article

Changes in Serum Levels of Matrix Metalloproteinase-1 and Tissue Inhibitor of Metalloproteinases-1 in Patients with Essential Hypertension

期刊

BIOENGINEERING-BASEL
卷 9, 期 3, 页码 -

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MDPI
DOI: 10.3390/bioengineering9030119

关键词

essential hypertension; matrix metalloproteinase-1; tissue inhibitor of metalloproteinases-1

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  1. Medical University-Pleven, Bulgaria

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This study investigated the serum levels of MMP-1 and TIMP-1 in patients with essential hypertension compared to normotensive individuals. The results showed significantly higher levels of MMP-1 and TIMP-1 in patients with hypertension compared to the control group. The elevated levels of MMP-1 in hypertension may be associated with increased collagen degradation in the cardiovascular extracellular matrix, while the increased levels of TIMP-1 may contribute to the pathological remodeling and fibrosis of the heart and arterial vessels.
Hypertension (HTN) is a leading risk factor for cardiovascular (CV) disease. Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are thought to be actively involved in the remodeling of the CV extracellular matrix (ECM) during hypertensive damage. Therefore, in this study, we aimed to investigate serum levels of MMP-1 and TIMP-1 in patients with essential HTN and compare them with those of normotensive individuals. We measured serum concentrations of MMP-1 and TIMP-1 in 60 patients with HTN and 20 healthy controls using an ELISA. The obtained results showed that in patients with HTN, the mean levels of MMP-1 (1.82 +/- 0.9 ng/mL) were significantly higher (p = 0.03) than the mean levels in the control group (1.19 +/- 0.7 ng/mL). The levels of TIMP-1 in patients with essential HTN (0.44 +/- 0.1 ng/mL) were also significantly higher (p = 0.005) than those in the control group (0.33 +/- 0.1 ng/mL). In HTN, elevated serum MMP-1 levels may be associated with increased collagen degradation in the CV ECM, whereas elevated TIMP-1 levels may favor its accumulation and the development of pathological remodeling and fibrosis of the heart and arterial vessels.

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