Novel anti-fibrotic effect of the UTP-sensitive P2Y11 receptor in rat cardiac myofibroblasts

Certal, Mariana; Vinhas, A.; Pinheiro, Ana Rita; Ferreirinha, Fátima; Ma, Costa; Correia‐de‐Sá, P.

doi:10.1016/j.autneu.2015.07.061

Cited by 2 publications

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“…P2Y 11 R agonists reduce cardiac fibrosis ( Certal et al, 2015 ). Extracellular nucleotide regulation of signalling in cardiac fibrosis has been discussed ( Novitskaya et al, 2016 ).…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Purinergic Signalling: Therapeutic Developments

2017

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Purinergic signalling, i.e., the role of nucleotides as extracellular signalling molecules, was proposed in 1972. However, this concept was not well accepted until the early 1990’s when receptor subtypes for purines and pyrimidines were cloned and characterised, which includes four subtypes of the P1 (adenosine) receptor, seven subtypes of P2X ion channel receptors and 8 subtypes of the P2Y G protein-coupled receptor. Early studies were largely concerned with the physiology, pharmacology and biochemistry of purinergic signalling. More recently, the focus has been on the pathophysiology and therapeutic potential. There was early recognition of the use of P1 receptor agonists for the treatment of supraventricular tachycardia and A2A receptor antagonists are promising for the treatment of Parkinson’s disease. Clopidogrel, a P2Y12 antagonist, is widely used for the treatment of thrombosis and stroke, blocking P2Y12 receptor-mediated platelet aggregation. Diquafosol, a long acting P2Y2 receptor agonist, is being used for the treatment of dry eye. P2X3 receptor antagonists have been developed that are orally bioavailable and stable in vivo and are currently in clinical trials for the treatment of chronic cough, bladder incontinence, visceral pain and hypertension. Antagonists to P2X7 receptors are being investigated for the treatment of inflammatory disorders, including neurodegenerative diseases. Other investigations are in progress for the use of purinergic agents for the treatment of osteoporosis, myocardial infarction, irritable bowel syndrome, epilepsy, atherosclerosis, depression, autism, diabetes, and cancer.

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“…P2Y 11 R agonists reduce cardiac fibrosis ( Certal et al, 2015 ). Extracellular nucleotide regulation of signalling in cardiac fibrosis has been discussed ( Novitskaya et al, 2016 ).…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Purinergic Signalling: Therapeutic Developments

2017

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“…143 P2Y 11 receptor agonists may be a means to reduce cardiac fibrosis. 144 A recent overview about extracellular nucleotide regulation of signaling in cardiac fibrosis has been published. 145 The P2X7 receptor antagonist, A740003, attenuates experimental autoimmune myocarditis and is promising for treating clinical myocarditis.…”

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confidence: 99%

Purinergic Signaling in the Cardiovascular System

Burnstock

2017

Circulation Research

339

295

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Abstract:There is nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory-motor nerves, as well as in intracardiac neurons. Centers in the brain control heart activities and vagal cardiovascular reflexes involve purines. Adenine nucleotides and nucleosides act on purinoceptors on cardiomyocytes, AV and SA nodes, cardiac fibroblasts, and coronary blood vessels. Vascular tone is controlled by a dual mechanism. ATP, released from perivascular sympathetic nerves, causes vasoconstriction largely via P2X1 receptors. Endothelial cells release ATP in response to changes in blood flow (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostaglandins to cause vasodilation. ATP is also released from sensory-motor nerves during antidromic reflex activity, to produce relaxation of some blood vessels. Purinergic signaling is involved in the physiology of erythrocytes, platelets, and leukocytes. ATP is released from erythrocytes and platelets, and purinoceptors and ectonucleotidases are expressed by these cells. P1, P2Y 1 , P2Y 12 , and P2X1 receptors are expressed on platelets, which mediate platelet aggregation and shape change. Long-term (trophic) actions of purine and pyrimidine nucleosides and nucleotides promote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and P2Y receptors during angiogenesis, vessel remodeling during restenosis after angioplasty and atherosclerosis. The involvement of purinergic signaling in cardiovascular pathophysiology and its therapeutic potential are discussed, including heart failure, infarction, arrhythmias, syncope, cardiomyopathy, angina, heart transplantation and coronary bypass grafts, coronary artery disease, diabetic cardiomyopathy, hypertension, ischemia, thrombosis, diabetes mellitus, and migraine. (Circ Res. 2017;120:207-228.

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Novel anti-fibrotic effect of the UTP-sensitive P2Y11 receptor in rat cardiac myofibroblasts

Cited by 2 publications

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Purinergic Signalling: Therapeutic Developments

Purinergic Signalling: Therapeutic Developments

Purinergic Signaling in the Cardiovascular System

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