About: Novel Anti-Thrombotic Mechanisms Mediated by Mas Receptor as Result of Balanced Activities Between the Kallikrein/Kinin and the Renin-Angiotensin Systems

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About: Novel Anti-Thrombotic Mechanisms Mediated by Mas Receptor as Result of Balanced Activities Between the Kallikrein/Kinin and the Renin-Angiotensin Systems Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Novel Anti-Thrombotic Mechanisms Mediated by Mas Receptor as Result of Balanced Activities Between the Kallikrein/Kinin and the Renin-Angiotensin Systems
Creator	Schmaier, Alvin Fang, Chao
source	Elsevier; Medline; PMC
abstract	The risk of thrombosis, a globally growing challenge and a major cause of death, is influenced by various factors in the intravascular coagulation, vessel wall, and cellular systems. Among the contributors to thrombosis, the contact activation system and the kallikrein/kinin system, two overlapping plasma proteolytic systems that are often considered as synonymous, regulate thrombosis from different aspects. On one hand, components of the contact activation system such as factor XII initiates activation of the coagulation proteins promoting thrombus formation on artificial surfaces through factor XI- and possibly prekallikrein-mediated intrinsic coagulation. On the other hand, physiological activation of plasma prekallikrein in the kallikrein/kinin system on endothelial cells liberates bradykinin from associated high-molecular-weight kininogen to stimulate the constitutive bradykinin B2 receptor to generate nitric oxide and prostacyclin to induce vasodilation and counterbalance angiotensin II signaling from the renin-angiotensin system which stimulates vasoconstriction. In addition to vascular tone regulation, this interaction between the kallikrein/kinin and renin-angiotensin systems has a thrombo-regulatory role independent of the contact pathway. At the level of the G-protein coupled receptors of these systems, defective bradykinin signaling due to attenuated bradykinin formation and/or decreased B2 receptor expression, as seen in murine prekallikrein and B2 receptor null mice, respectively, leads to compensatory overexpressed Mas, the receptor for angiotensin-(1-7) of the renin-angiotensin system. Mas stimulation and/or its increased expression contributes to maintaining a healthy vascular homeostasis by generating graded elevation of plasma prostacyclin which reduces thrombosis through two independent pathways: (1) increasing the vasoprotective transcription factor Sirtuin 1 to suppress tissue factor expression, and (2) inhibiting platelet activation. This review will summarize the recent advances in this field that support these understandings. Appreciating these subtle mechanisms help to develop novel anti-thrombotic strategies by targeting the vascular receptors in the renin-angiotensin and the kallikrein/kinin systems to maintain healthy vascular homeostasis.
has issue date	2020-07-24(xsd:dateTime)
bibo:doi	10.1016/j.phrs.2020.105096
bibo:pmid	32712319
has license	no-cc
sha1sum (hex)	f050492bf7ab052cb1ef9942716773b1538e2cc3
schema:url	https://doi.org/10.1016/j.phrs.2020.105096
resource representing a document's title	Novel Anti-Thrombotic Mechanisms Mediated by Mas Receptor as Result of Balanced Activities Between the Kallikrein/Kinin and the Renin-Angiotensin Systems
has PubMed Central identifier	PMC7378497
has PubMed identifier	32712319
schema:publication	Pharmacol Res
resource representing a document's body	covid:f050492bf7ab052cb1ef9942716773b1538e2cc3#body_text
is schema:about of	named entity 'Mas' named entity 'Result' named entity 'Novel' named entity 'Mechanisms' named entity 'Journal' named entity 'Kallikrein' named entity 'Balanced' named entity 'Renin-Angiotensin' named entity 'bdkrb2' named entity 'agonist' named entity 'thrombin' named entity 'PGI2' named entity 'kininogen' named entity 'exogenous' named entity 'kininogen' named entity 'BDKRB2' named entity 'BDKRB2' named entity 'active form' named entity 'direct thrombin inhibitor' named entity 'AT1R' named entity 'factor XI' named entity 'platelet' named entity 'COX-2' named entity 'thrombin' named entity 'platelet' named entity 'SIRT1' named entity 'PPARβ/δ' named entity 'thrombomodulin' named entity 'endothelial cells' named entity 'Ang II' named entity 'SIRT3' named entity 'nimesulide' named entity 'prekallikrein' named entity 'COX-2' named entity 'klkb1' named entity 'prekallikrein' named entity 'kallikrein' named entity 'plasma' named entity 'tissue factor' named entity 'kininogen' named entity 'collagen' named entity 'homolog' named entity 'plasma' named entity 'thrombosis' named entity 'nicotinamide adenine dinucleotide' named entity 'klkb1' named entity 'anti-thrombotic' named entity 'proteolytic' named entity 'kinin' named entity 'histones' named entity 'angiotensin II receptor type 2' named entity 'SIRT1' named entity 'thrombosis' named entity 'PGI2' named entity 'COX-2' named entity 'thrombus' named entity 'BDKRB2' named entity 'fibrinolytic' named entity 'ACE' named entity 'klkb1' named entity 'CK1' named entity 'vascular homeostasis' named entity 'keto' named entity 'plasma' named entity 'prekallikrein' named entity 'Ang II' named entity 'peptide' named entity 'physiological' named entity 'PGI2' named entity 'bradykinin' named entity 'transcription factor' named entity 'PGI2' named entity 'deacetylation' named entity 'kinin' named entity 'pharmacological' named entity 'thrombus' named entity 'Physiological' named entity 'antigens' named entity 'endothelial cells' named entity 'AT1R'

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