Matrix metalloproteinases: role in the development of myocardial postinfarction remodeling

Прудников, А. Р.; Schupakova, A. N.

doi:10.24884/1682-6655-2018-17-1-13-24

Cited by 2 publications

(1 citation statement)

References 47 publications

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“…[20]. Аналогичные процессы, обуславливающие ремоделирование миокарда у больных АГ с высоким ССР, также регулируются ММП, но другими их подтипами [21].…”

Section: Discussionunclassified

Content of matrix metalloproteinases in the blood of hypertensive patients with a high cardiovascular risk receiving statin therapy

Михин

Осипова

Vorotyntseva

et al. 2022

Cardiovasc Ther Prev

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Aim. To compare the effect of atorvastatin and rosuvastatin as part of complex therapy in patients with hypertension (HTN) with a high cardiovascular risk on the level of matrix metalloproteinases -1, -9 (MMP-1, MMP-9) and tissue inhibitors of metalloproteinases -1, -4 (TIMP-1, TIMP-4).Material and methods. The study included 140 hypertensive patients who received atorvastatin (Liprimar) 20 mg/day in addition to antihypertensive therapy for a year, which was later replaced by rosuvastatin (Rosucard) in the following doses: 10 mg/day (n=96), 20 mg/day (n=24), 40 mg/day (n=26). Patients underwent standard clinical and paraclinical investigations. In the blood serum of patients, the levels of MMP-1, MMP-9 and TIMP-1, TIMP-4 were determined.Results. Patients who used rosuvastatin at a dose of 40 mg/day had a more pronounced decrease in MMP-1 than those treated with rosuvastatin at a dose of 10 and 20 mg/day (p<0,05), while there were no differences in MMP-1 when using low and medium doses. Rosuvastatin had a less pronounced effect on MMP-9 than on MMP-1, while increasing the dose of rosuvastatin did not affect the intensity of MMP-9 reduction (p>0,05). The content of TIMP-1 and TIMP-4 increased when taking rosuvastatin, while a more pronounced dose-dependent increase in TIMP-1 was observed with rosuvastatin 20 mg/day and 40 mg/day. In addition, the largest increase in TIMP-4 was observed when using rosuvastatin at a dose of 40 mg/day. Atorvastatin had no significant effect on MMP-1 and MMP-9, as well as TIMP-1 and TIMP-4.Conclusion. Long-term rosuvastatin therapy (10 mg/day, 20 mg/day, 40 mg/day) as part of the complex therapy of cardiovascular patients affects the metabolism of vascular wall elastin and collagen, reducing the level of MMP-1, MMP-9 and increasing the content of TIMP-1, TIMP-4 in the blood.

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Section: Discussionunclassified

Content of matrix metalloproteinases in the blood of hypertensive patients with a high cardiovascular risk receiving statin therapy

Михин

Осипова

Vorotyntseva

et al. 2022

Cardiovasc Ther Prev

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The mechanisms of the extracellular matrix remodeling of myocardium among patients with hypertension

Kulbachuk,

Sid,

Soloviov

et al. 2023

Rep. of Vinnytsia Nation. Med. Univ.

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Annotation. The present review article highlights the central mechanisms that contribute to the extracellular matrix remodeling in the myocardium among patients with hypertension. Based on the scientometric databases Web of Science, Scopus, and PubMed, a retrospective analysis of the literature issued in 2010-2022 on this specific topic was conducted. After reviewing the article abstracts and getting acquainted with their full text, we selected 30 sources. The search results suggest that under physiological conditions, collagen ensures structural integrity by preventing excessive stretching of cardiomyocytes. It was established in the course of the research that progressive vascular fibrosis occurs due to excessive collagen synthesis relative to its degradation by metalloproteinases. Metalloproteinases play a central role in the exchange of connective tissue proteins. Cytokinins such as tumor necrosis factor alpha and interleukin-1β contribute to the accumulation of collagen in the intercellular space, aldosterone being another contributor to the process. It has been noted that hypertensive disease is associated with high activity of angiotensin-II, which regulates the expression of β-transforming growth factor and has pro-fibrotic properties. Biological molecules of catecholamines, as well as molecules of aldosterone and angiotensin-II, affect the activity of MMP by suppressing NO activity in the vessel wall. An understanding of various pathophysiological mechanisms involved in hypertension leading to vascular dysfunction and myocardial remodeling as well as changes in the extracellular matrix of the myocardium can prove to be essential for identifying critical pharmacological targets. The priority of prescribing specific groups of antihypertensive drugs remains uncertain at the moment, but special attention is paid to their effect on the inhibition and reversal of the development of myocardial and vascular fibrosis. Thus, the study of the activity of enzymes of the metalloproteinase family is promising for clinical studies in hypertension.

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Matrix metalloproteinases: role in the development of myocardial postinfarction remodeling

Cited by 2 publications

References 47 publications

Content of matrix metalloproteinases in the blood of hypertensive patients with a high cardiovascular risk receiving statin therapy

Content of matrix metalloproteinases in the blood of hypertensive patients with a high cardiovascular risk receiving statin therapy

The mechanisms of the extracellular matrix remodeling of myocardium among patients with hypertension

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