Extracellular atp contributes to atherogenesis via purinergic receptors by inducing leukocyte recruitment in mice

Stachon, Peter; Hergeth, S.H.; Michel, Noémie; Dufner, Bianca; Rodríguez, Arturo Rodríguez; Hoppe, Natalie; Wolf, Dennis; Bode, Christoph; Idzko, Marco; Zirlik, Andreas

doi:10.1093/eurheartj/eht308.p2393

Cited by 4 publications

(3 citation statements)

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“…Extracellular ATP and ADP at micromolar concentrations lead to impaired production of interferon-γ and IL-12 in leukocytes in the lipopolysaccharide-stimulated whole human blood model of sepsis [399]. ATP contributes to atherogenesis, via P2Y 2 , P2Y 6 , P2X4 and P2X7 receptors by inducing leukocyte recruitment in mice [400]. Abacavir is linked to cardiovascular disease, and ATP has been shown to play a role in leukocyte accumulation induced by abacavir, via P2X7 receptors [401].…”

Section: Leukocytesmentioning

confidence: 99%

Blood cells: an historical account of the roles of purinergic signalling

Burnstock

2015

Purinergic Signalling

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The involvement of purinergic signalling in the physiology of erythrocytes, platelets and leukocytes was recognised early. The release of ATP and the expression of purinoceptors and ectonucleotidases on erythrocytes in health and disease are reviewed. The release of ATP and ADP from platelets and the expression and roles of P1, P2Y 1 , P2Y 12 and P2X1 receptors on platelets are described. P2Y 1 and P2X1 receptors mediate changes in platelet shape, while P2Y 12 receptors mediate platelet aggregation. The changes in the role of purinergic signalling in a variety of disease conditions are considered. The successful use of P2Y 12 receptor antagonists, such as clopidogrel and ticagrelor, for the treatment of thrombosis, myocardial infarction and stroke is discussed.

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Section: Leukocytesmentioning

confidence: 99%

Blood cells: an historical account of the roles of purinergic signalling

Burnstock

2015

Purinergic Signalling

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“…ATP, acting mainly via metabotropic P2Y receptors, has potent mitogenic and pro-inflammatory effects involved in stepwise formation of atheroma plaques [81]. Evidence also exists on direct involvement of P2X receptors in atherosclerosis [81,128,129]. For instance, upregulation of endothelial P2X4R and/or P2X7R has been observed in response to cellular damage inflicted by dyslipidemia and hyperglycemia; overactivation of these receptors has been linked to the release of pro-inflammatory cytokines and increases in endothelial permeability [130].…”

Section: Cardiovascular Risk Factors: Is the P2x4 Receptor Friend Or mentioning

confidence: 99%

Resolving the Ionotropic P2X4 Receptor Mystery Points towards a New Therapeutic Target for Cardiovascular Diseases

Bragança

Correia-de-Sá

2020

IJMS

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Adenosine triphosphate (ATP) is a primordial versatile autacoid that changes its role from an intracellular energy saver to a signaling molecule once released to the extracellular milieu. Extracellular ATP and its adenosine metabolite are the main activators of the P2 and P1 purinoceptor families, respectively. Mounting evidence suggests that the ionotropic P2X4 receptor (P2X4R) plays pivotal roles in the regulation of the cardiovascular system, yet further therapeutic advances have been hampered by the lack of selective P2X4R agonists. In this review, we provide the state of the art of the P2X4R activity in the cardiovascular system. We also discuss the role of P2X4R activation in kidney and lungs vis a vis their interplay to control cardiovascular functions and dysfunctions, including putative adverse effects emerging from P2X4R activation. Gathering this information may prompt further development of selective P2X4R agonists and its translation to the clinical practice.

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“…113 Recent studies have also demonstrated that ATP enhances macrophage lipid deposition and migration 114 and contributes to atherogenesis via purinergic receptors by inducing leukocyte recruitment in mice. 115 Serum uric acid levels have been shown to predict the severity and morphology of coronary atherosclerosis, 116 as well as the progression of subclinical coronary artery disease. 117 Similar to ATP, the acute release of uric acid after cell death can lead to an inflammatory response in surrounding immune cells.…”

Section: Cell Deathmentioning

confidence: 99%

Danger Signaling in Atherosclerosis

Zimmer

Grebe

Latz

2015

Circulation Research

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All aspects of the pathogenesis of atherosclerosis are critically influenced by the inflammatory response in vascular plaques. Research in the field of innate immunity from the past 2 decades has uncovered many novel mechanisms elucidating how immune cells sense microbes, tissue damage, and metabolic derangements. Here, we summarize which triggers of innate immunity appear during atherogenesis and by which pathways they can contribute to inflammation in atherosclerotic plaques. The increased understanding gained from studies assessing how immune activation is associated with the pathogenesis of atherosclerosis has provided many novel targets for potential therapeutic intervention. Excitingly, the concept that inflammation may be the core of cardiovascular disease is currently being clinically evaluated and will probably encourage further studies in this area.

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Extracellular atp contributes to atherogenesis via purinergic receptors by inducing leukocyte recruitment in mice

Cited by 4 publications

References 0 publications

Blood cells: an historical account of the roles of purinergic signalling

Blood cells: an historical account of the roles of purinergic signalling

Resolving the Ionotropic P2X4 Receptor Mystery Points towards a New Therapeutic Target for Cardiovascular Diseases

Danger Signaling in Atherosclerosis

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