Abstract
Gelatinases (matrix metalloproteinase-2 and -9) are enzymes from the matrix metalloproteinases (MMPs) family, which are associated with collagen degradation. MMP-2 is capable of cleaving gelatine, types I and IV collagens, while MMP-9 is incapable of direct proteolysis of collagen I and digests collagen type IV. MMP-2 and -9 are both important regulators of vascular and uterine remodeling in a healthy pregnancy. Alterations in the collagen structure of the uterus and spiral arteries are observed in women with hypertensive disorders of pregnancy. Dysregulation of MMP-2 and MMP-9 has been implicated in abnormal vasodilation, placentation, and uterine expansion in preeclampsia. Early preeclampsia detection is paramount for risk stratification and prevention of further complications. Understanding the role of MMP-2 and-9 in uteroplacental and vascular remodeling could help design new approaches for prediction and management of preeclampsia. This review presents a general survey of MMP-2 and MMP-9 faulty regulation and impaired collagen types I and IV turnover in complicated pregnancies. Their potential role as circulating markers for diagnosis, prognosis, and monitoring of preeclampsia development is discussed as well.
Highlights
Received: 30 January 2021Accepted: 4 March 2021Published: 9 March 2021Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Licensee MDPI, Basel, Switzerland.Preeclampsia (PE) is one of the most significant causes of maternal and perinatal morbidity and mortality
matrix metalloproteinases (MMPs)-2 and MMP-9 are frequently implicated as important factors that contribute to the cytotrophoblast invasion into the maternal vasculature
In order to evaluate whether dimerization of matrix metalloproteinases plays a role in hypertensive pregnancy (HTN-Preg) and intrauterine growth restriction (IUGR) Chen et al, 2017, measured the levels/activity of MMP-9, tissue inhibitor of metalloproteinase (TIMP-1), and their dimerization forms in the placenta, uterus, and uterine artery of normal pregnant rats and a rat model of reduction of uterine perfusion pressure (RUPP)
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Preeclampsia (PE) is one of the most significant causes of maternal and perinatal morbidity and mortality. It has been estimated that around 2–8 per cent of pregnancies in the world are complicated by PE. The mechanisms of PE have not yet been clearly identified. There is evidence that vascular resistance is abnormally increased and leads to hypertension in women with PE, but the causal mechanisms leading to preeclampsia have not yet been fully estimated. Poor placental perfusion plays an important role in increasing maternal vascular resistance, it has been proposed as a significant reason for subsequent placental ischemia. Studies have demonstrated placental ischemia and hypoxia as a central causative factor in the etiology of preeclampsia. Altered placental perfusion has been highlighted as a major reason leading to widespread maternal endothelial dysfunction
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