Vascular functions of the plasminogen activation system




















Methods Citations. Figures and Topics from this paper. Citation Type. Has PDF. Publication Type. More Filters. Use of mouse models to study plasminogen activator inhibitor Methods in enzymology. Regulation of arterial remodeling and angiogenesis by urokinase-type plasminogen activator.

Canadian journal of physiology and pharmacology. Three decades of research on plasminogen activator inhibitor a multifaceted serpin. Seminars in thrombosis and hemostasis. Journal of molecular and genetic medicine : an international journal of biomedical research. View 1 excerpt, cites background. Thrombosis research. Plasminogen activator inhibitor-1 PAI-1 : a key factor linking fibrinolysis and age-related subclinical and clinical conditions. Cardiovascular therapeutics.

The role of the annexin A2 heterotetramer in vascular fibrinolysis. Plasmin as a proinflammatory cell activator. Journal of leukocyte biology. View 2 excerpts, cites background. Plasminogen activator inhibitor 1, fibrin, and the vascular response to injury.

Trends in cardiovascular medicine. Regulation and interactions in the activation of cell-associated plasminogen. Medicina Kaunas , 57 7 , 25 Jun Protein Sci , 30 3 , 13 Jan Cited by: 1 article PMID: J Cardiovasc Transl Res , 14 1 , 16 Jun Biofactors , 46 2 , 04 Sep Free to read. To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.

Methods Enzymol , , 01 Jan Cited by: 7 articles PMID: Thromb Haemost , 6 , 01 Dec Cited by: 41 articles PMID: Thromb Haemost , 87 6 , 01 Jun Cited by: 5 articles PMID: Trends Cardiovasc Med , 14 5 , 01 Jul Cited by: 31 articles PMID: Rev Prat , 47 20 , 01 Dec Cited by: 2 articles PMID: Contact us.

Europe PMC requires Javascript to function effectively. Recent Activity. Search life-sciences literature Over 39 million articles, preprints and more Search Advanced search. This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our privacy notice and cookie policy. Abstract Read article for free, via Unpaywall a legal, open copy of the full text.

Fay WP ,. Nadish Garg Search articles by 'Nadish Garg'. Garg N ,. Madhavi Sunkar Search articles by 'Madhavi Sunkar'. Sunkar M. Affiliations All authors 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract The plasminogen activator PA system, which controls the formation and activity of plasmin, plays a key role in modulating hemostasis, thrombosis, and several other biological processes. While a great deal is known about the function of the PA system, it remains a focus of intensive investigation, and the list of biological pathways and human diseases that are modulated by normal and pathologic function of its components continues to lengthen.

Because of remarkable advances in molecular genetics, the laboratory mouse has become the most useful animal system to study the normal and pathologic functions of the PA system. The purpose of this review is to summarize studies that have used genetically modified mice to examine the functions of the PA system in hemostasis and thrombosis, intimal hyperplasia after vascular injury, and atherosclerosis.

Particular emphasis is placed on the vascular functions of PA inhibitor-1, a key regulator of the PA system, and the multiple variables that appear to account for the complex role of PA inhibitor-1 in regulating vascular remodeling. Lastly, the strengths and limitations of using mice to model human vascular disease processes are discussed.

References Articles referenced by this article 86 Regulation and interactions in the activation of cell-associated plasminogen. Molecular mechanisms of fibrinolysis. Plasminogen receptors: the sine qua non of cell surface plasminogen activation.

Plasminogen activator inhibitor 1, fibrin, and the vascular response to injury. Plasminogen enhances virulence of group A streptococci by streptokinase-dependent and streptokinase-independent mechanisms. Plasminogen is a critical host pathogenicity factor for group A streptococcal infection. Bacterial metastasis: the host plasminogen system in bacterial invasion. Show 10 more references 10 of



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