Список литературы

2687-0940

Актуальные проблемы медицины

2687-0940

10.18413/2687-0940-2020-43-3-392-403

КАРДИОЛОГИЯ

Матриксные металлопротеиназы и их роль в развитии ремоделирования у больных, перенесших острый инфаркт миокарда (обзор литературы)

Matrix metalloproteinases and their role in the development of remodeling in patients with acute myocardial infarction (review of literature)

Букатов

Владислав Владимирович

Bukatov

Vladislav V.

2020

43300

Особый интерес представляют собой механизмы ремоделирования миокарда после перенесенного инфаркта миокарда (ИМ). К сожалению, на сегодняшний день у науки нет однозначного ответа на вопрос о процессе ремоделирования миокарда после ИМ. Так, например, у двух схожих клинически пациентов, без сопутствующих заболеваний, с одинаковой локализацией ИМ, схожим временем открытия коронарной артерии в отдаленном периоде развивается совершенно разная картина сердечной недостаточности. У одного происходит дилатация полостей сердца, снижение фракции выброса, а у другого совершенно отсутствуют проявления сердечной недостаточности. Относительно недавно был установлен факт влияния матриксных металлопротеиназ на протекание ИМ, резкое повышение их концентрации в острый и отдаленный период наводят на рассуждения о их важнейшей роли в процессах ремоделирования миокарда. Настоящий обзор попытался обобщить полученные данные о роли матриксных металлопротеиназ и ИМ и выявить существующую закономерность.

The mechanisms of myocardial remodeling after myocardial infarction (MI) are of particular interest. Unfortunately, today science does not have an unambiguous answer to the question about the process of myocardial remodeling after MI. For example, in two clinically similar patients, without concomitant diseases, with the same localization of myocardial infarction, with a similar opening time of the coronary artery, in the long-term period, a completely different picture of heart failure develops, one has dilatation of the heart cavities, a decrease in the ejection fraction, and the other has absolutely no manifestations heart failure. Relatively recently, the fact of the influence of matrix metalloproteinases on the course of myocardial infarction was established; a sharp increase in their concentration in the acute and long-term period suggests speculation about their most important role in the processes of myocardial remodeling. In this review, we tried to summarize the existing data on the role of matrix metalloprotenases and MI, and tried to identify the existing pattern.

инфаркт миокардаремоделирование миокардахроническая сердечная недостаточностьматриксные металлопротеиназы

myocardial infarctionmyocardial remodelingchronic heart failurematrix metalloproteinases

Список литературы

Фомин И.В. 2016. Хроническая сердечная недостаточность в Российской Федерации: что сегодня мы знаем и что должны делать. Российский кардиологический журнал. 8: 7–13.

A. Deten, H.C. Volz, W. Briest, H. Zimmer. 2002. Cardiac cytokine expression is upregulated in the acute phase after myocardial infarction. Experimental studies in rats. Cardiovasc Res. 55: 329–340

Andrew D. Rouillard, Jeffrey W. Holmes. 2012. Mechanical regulation of fibroblast migration and collagen remodeling in healing myocardial infarcts. The Journal of Physiology. 15; 590 (18): 4585–4602. doi: 10.1113/jphysiol.2012.229484.

Andrew P. Voorhees, Kristine Y. DeLeon-Pennell, Yonggang Ma, Ganesh V. Halade, Andriy Yabluchanskiy, Rugmani Padmanabhan Iyer , Elizabeth Flynn, Courtney A. Cates , Merry L. Lindsey, Hai-Chao Han. 2015. Building a Better Infarct: Modulation of Collagen Cross-linking to Increase Infarct Stiffness and Reduce Left Ventricular Dilation post-Myocardial Infarction. J. Mol. Cell. Cardiol. 85: 229–239. doi:10.1016/j.yjmcc.2015.06.006.

Anita M. Tuomainen, Kristiina Nyyssönen, Jari A. Laukkanen, Taina Tervahartiala, Tomi-Pekka Tuomainen, Jukka T. Salonen, Timo Sorsa, Pirkko J. Pussinen. 2007. Matrix metalloproteinase-8 concentrations are associated with cardiovascular outcome in men. Serum Arteriosclerosis, Thrombosis, and Vascular Biology. 27 (12): 2722–272. doi: 10.1161/ATVBAHA.107.154831.

Barak Marom, Michal A., Rahat Nitza Lahat Lea Weiss Cerem, Amalia Kinarty, Haim Bitterman. 2007. Native and fragmented fibronectin oppositely modulate monocyte secretion of MMP-9. Journal of Leukocyte Biology. 81: 1466–1476.

Ben Fogelgren, Noémi Polgár, Kornélia Molnárné Szauter, Zsuzsanna Ujfaludi, Rozália Laczkó, Keith S. K. Fong, Katalin Csiszar. 2005. Cellular Fibronectin Binds to Lysyl Oxidase with High Affinity and Is Critical for Its Proteolytic Activation. Journal of Biological Chemistry. 280: 24690–24697.

Carson S. Webb, David D. Bonnema, S. Hinan Ahmed, Amy H. Leonardi, Catherine D. McClure, Leslie L. Clark, Robert E. Stroud, William C. Corn, Laura Finklea, Michael R. Zile, Francis G. Spinale. 2006. Specific temporal profile of matrix metalloproteinase release occurs in patients after myocardial infarction: relation to left ventricular remodeling. Circulation. 114: 1020–1027. doi: 10.1161/CIRCULATIONAHA.105.600353.

Dominic Kelly, Gillian Cockerill, Leong L. Ng, Matt Thompson, Sohail Khan, Nilesh J. Samani, Iain B. Squire. 2007. Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study. Eur. Heart. J. Mar. 28 (6): 711–718. doi:10.1093/eurheartj/ehm003.

Dominic Kelly, Sohail Q. Khan, Matt Thompson, Gillian Cockerill, Leong L. Ng, Nilesh Samani, Lain B. Squire. Plasma tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-9.2008. Novel indicators of left ventricular remodelling and prognosis after acute myocardial infarction. Eur Heart J. 29 (17): 2116–2124. doi: 10.1093/eurheartj/ehn315.

Giulia Angelini, Davide Flego, Ramona Vinci, Daniela Pedicino, Francesco Trotta, Aureliano Ruggio, Giuseppe P. Piemontese, Domenico Galante, Myriana Ponzo, Luigi M. Biasucci, Giovanna Liuzzo, Filippo Crea. 2018. Matrix metalloproteinase-9 might affect adaptive immunity in non-ST segment elevation acute coronary syndromes by increasing CD31 cleavage on CD4+ T-cells. Eur. Heart. J. 39(13): 1089–1097. doi: 10.1093/eurheartj/ehx684.

Hatem Alfakry, Juha Sinisalo, Susanna Paju, Markku S. Nieminen, Ville Valtonen, Taina Tervahartiala, Pirkko J. Pussinen, Timo Sorsa. 2012. The association of serum neutrophil markers and acute coronary syndrome. Scandinavian Journal of Immunology. 76 (2): 181–187. doi: 10.1111/j.1365-3083.2012.02718.x.

K. J. Molloy, M. M. Thompson, J. L. Jones, E. C. Schwalbe, P. R. F. Bell, A. R .Naylor, I. M. Loftus. 2004. Unstable carotid plaques exhibit raised matrix metalloproteinase-8. Circulation. 110 (3): 337–340 doi: 10.1161/01.CIR.0000135588.65188.14.

Khalil A. 2018. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease Advances in Pharmacology. 81: 241–330. DOI: 10.1016/bs.apha.2017.08.002.

Kristine Y. Deleon-Pennell, Raffaele Altara, Andriy Yabluchanskiy, Alessandra Modesti, Merry L. Lindsey. 2015. The Circular Relationship between Matrix Metalloproteinase (MMP)-9 and Inflammation following Myocardial Infarction. IUBMB Life.67 (8): 611–618. doi: 10.1002/iub.1408.

Kristine Y. DeLeon-Pennell, Yuan Tian, Bai Zhang, Courtney A. Cates, Rugmani Padmanabhan Iyer, Presley Cannon, Punit Shah, Paul Aiyetan, Ganesh V. Halade, Yonggang Ma, Elizabeth Flynn, Zhen Zhang, Yu-Fang Jin, Hui Zhang, Merry L. Lindsey. 2016. CD36 is a matrix metalloproteinase-9 substrate that stimulates neutrophil apoptosis and removal during cardiac remodeling. Circ. Cardiovasc. Genet. 9: 14–25.

M. Lindsey, K. Wedin, M. D. Brown, C. Keller, A. J. Evans, J. Smolen, A. R. Burns, R. D. Rossen, L. Michael, M. Entman. 2001. Matrix-dependent mechanism of neutrophil-mediated release and activation of matrix metalloproteinase 9 in myocardial ischemia/reperfusion. Circulation. 103:2181–2187.

Marta Miguel Turu, Jerzy Krupinski, Esther Catena, Ana Rosell, Joan Montaner, Francisco Rubio, Jose Alvarez-Sabin, Marc Cairols, Lina Badimon. 2006. Intraplaque MMP-8 levels are increased in asymptomatic patients with carotid plaque progression on ultrasound. Atherosclerosis. 187 (1): 161–169. doi: 10.1016/j.atherosclerosis.2005.08.039.

Monika Pavkova Goldbergova, Jiri Parenica, Jiri Jarkovsky, Petr Kala, Martin Poloczek, Jan Manousek, Krystyna Kluz, Lenka Kubkova, Simona Littnerova, Martin Tesak, Ondrej Toman, Nikolas Pavek, Zdenka Cermakova, Josef Tomandl, Anna Vasku, Jindrich Spinar. 2012. The Association Between Levels of Tissue Inhibitor of Metalloproteinase-1 with Acute Heart Failure and Left Ventricular Dysfunction in Patients with ST Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention. Genet. Test. Mol. Biomarkers.16 (10): 1172–1178. doi:10.1089/gtmb.2012.0120.

Ohuchi E., Imai K., Fujii Y., Sato H., Seiki M,. Okada Y. 1997. Membrane type 1 matrix metalloproteinase digests interstitial collagens and other extracellular matrix macromolecules. Biol Chem 24; 272(4) 2446-2451. doi: 10.1074/jbc.272.4.2446.

Rogelio Zamilpa, Elizabeth F. Lopez, Ying Ann Chiao, Qiuxia Dai, Gladys P. Escobar, Kevin Hakala, Susan T. Weintraub, Merry L. Lindsey. 2010. Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction. Proteomics. 10: 2214–2223.

Rogelio Zamilpa, Jessica Ibarra, Lisandra E. de Castro Brás, Trevi A. Ramirez, Nguyen Nguyen, Ganesh V. Halade, Jianhua Zhang, Qiuxia Dai, Tariq Dayah, Ying Ann Chiao, Wesley Lowell, Seema S. Ahuja, Jeanine D’Armiento, Yu-Fang Jin, Merry L. Lindsey. 2012. Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. J. Mol. Cell. Cardiol. 53: 599–608.

Rogelio Zamilpa, Jessica Ibarra, Lisandra E. de Castro Brás, Trevi A. Ramirez, Nguyen Nguyen, Ganesh V. Halade, Jianhua Zhang, Qiuxia Dai, Tariq Dayah, Ying Ann Chiao, Wesley Lowell, Seema S. Ahuja, Jeanine D’Armiento, Yu-Fang Jin, and Merry L. Lindsey, Ph.D. 2012. Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. J. Mol. Cell. Cardiol. 53: 599–608.

Rugmani Padmanabhan Iyer, Mira Jung, Merry L. Lindsey. 2016. MMP-9 signaling in the left ventricle following myocardial infarction. Am. J. Physiol. Heart. Circ. Physiol. 311 (1): 190–198. doi:10.1152/ajpheart.00243.

Takahiko Naruko, Makiko Ueda, Kazuo Haze, Allard C. van der Wal, Chris M. van der Loos, Akira Itoh, Ryushi Komatsu, Yoshihiro Ikura, Masayuki Ogami, Yoshihisa Shimada, Shoichi Ehara, Minoru Yoshiyama, Kazuhide Takeuchi, Junichi Yoshikawa, Anton E. Becker. 2002. Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation. 106 (23): 2894–2900. doi: 10.1161/01.cir.0000042674.89762.20.

V. Knäuper, G. Murphy, H. Tschesche. 1996. Activation of human neutrophil procollagenase by stromelysin 2. European Journal of Biochemistry. 235 (1–2): 187–191.

Yukihiko Momiyama, Reiko Ohmori, Nobukiyo Tanaka, Ryuichi Kato, Hiroaki Taniguchi, Takeshi Adachi, Haruo Nakamura, Fumitaka Ohsuzu. 2010. High plasma levels of matrix metalloproteinase-8 in patients with unstable angina. Atherosclerosis. 209 (1): 206–210. DOI: https://doi.org/10.1016/j.atherosclerosis.2009.07.037.