Increase in tissue endothelin-1 and ETA receptor levels in human aortic valve stenosis

Peltonen, T; Taskinen, Panu; Näpänkangas, Juha; Leskinen, Hanna; Ohtonen, Pasi; Soini, Ylermi; Juvonen, Tatu; Satta, Jari; Vuolteenaho, Olli; Ruskoaho, Heikki

doi:10.1093/eurheartj/ehn482

Cited by 43 publications

(34 citation statements)

References 35 publications

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“…In man, apelin peptide is up-regulated in atherosclerotic coronary ar-APELIN RECEPTOR NOMENCLATURE 337 tery , and both apelin and its receptor are up-regulated in aortic valve stenosis, a process that displays some hallmarks of atherosclerosis (Peltonen et al, 2009), supporting an involvement of the apelin system in human atherosclerosis. Apelin also prevents aortic aneurism formation in mice (Leeper et al, 2009).…”

Section: A Cardiovascular Diseasementioning

confidence: 97%

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Pitkin

Maguire²,

Bonner³

et al. 2010

Pharmacol Rev

164

133

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Section: A Cardiovascular Diseasementioning

confidence: 97%

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Pitkin

Maguire²,

Bonner³

et al. 2010

Pharmacol Rev

164

133

View full text Add to dashboard Cite

“…Indeed, apelin-13, an important active form, was up-regulated in human atherosclerotic coronary artery and this additional peptide was localized to the plaque, co-localizing with markers for macrophages and smooth muscle cells [8]. Moreover, in calcified aortic valve disease patients, the gene expression of apelin and the APJ receptor were shown to be significantly up-regulated in stenotic valves [9]. Which factors cause the overexpression as well as the role of apelin in AS is worth being further studied.…”

Section: Expression and Location Of Apelin/apj In Atherosclerosis Patmentioning

confidence: 98%

Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Lv¹,

Li²,

Chen³

2013

ABBS

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Apelin is a bioactive peptide discovered recently that has been proved to be an endogenous ligand of the APJ receptor. Apelin and APJ are widely distributed in the central nervous system and peripheral tissues. Researches have confirmed that apelin/APJ involved in a wide range of physiological and pathological functions in the cardiovascular system. Investigations indicated that apelin is a novel critical factor in the development of atherosclerosis (AS). In this review, we discuss the roles of apelin in the vascular smooth muscle cell proliferation, monocytes-endothelial cell adhesion, and angiogenesis that potentially reveals a new cellular mechanism of AS. Considering these roles, apelin and APJ may be novel therapeutic targets of AS.

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“…These molecules play an important role in the development and progression of atherosclerosis and the formation of occlusive thrombi. 4 Apelin and its cognate receptor APJ were shown to be involved in a number of physiological and pathophysiological conditions, 5 and their levels are altered in atherosclerotic coronary arteries, 6 in aortic valve stenosis, 7 and during acute myocardial infarction and angina. [8][9][10] All these observations raise the possibility that apelin signaling pathways play a role in the physiopathology of vascular disease.…”

Section: Introductionmentioning

confidence: 99%

Apelin: an antithrombotic factor that inhibits platelet function

Adam

Khatib

López

et al. 2016

Blood

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Key Points• Apelin plays a key role in maintaining hemostasis through the regulation of platelet function.• Treatment of platelets with apelin inhibits aggregation and thrombus formation.Apelin peptide and its receptor APJ are directly implicated in various physiological processes ranging from cardiovascular homeostasis to immune signaling. Here, we show that apelin is a key player in hemostasis with an ability to inhibit thrombin-and collagenmediated platelet activation. Mice lacking apelin displayed a shorter bleeding time and a prothrombotic profile. Their platelets exhibited increased adhesion and a reduced occlusion time in venules, and displayed a higher aggregation rate after their activation by thrombin compared with wild-type platelets. Consequently, human and mouse platelets express apelin and its receptor APJ. Apelin directly interferes with thrombin-mediated signaling pathways and platelet activation, secretion, and aggregation, but not with ADP and thromboxane A 2 -mediated pathways. IV apelin administration induced excessive bleeding and prevented thrombosis in mice. Taken together, these findings suggest that apelin and/or APJ agonists could potentially be useful adducts in antiplatelet therapies and may provide a promising perspective for patients who continue to display adverse thrombotic events with current antiplatelet therapies. (Blood. 2016;127(7):908-920)

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Increase in tissue endothelin-1 and ETA receptor levels in human aortic valve stenosis

Abstract: AS is characterized by distinct upregulation of ET-1 and its target receptor ET(A), promoting growth, inflammation, and fibrosis. These findings suggest therapeutic potential for ET(A)-receptor antagonists in aortic valve calcification.

Cited by 43 publications

References 35 publications

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

International Union of Basic and Clinical Pharmacology. LXXIV. Apelin Receptor Nomenclature, Distribution, Pharmacology, and Function

Apelin and APJ, a novel critical factor and therapeutic target for atherosclerosis

Apelin: an antithrombotic factor that inhibits platelet function

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