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- W2135087274 endingPage "1016" @default.
- W2135087274 startingPage "1007" @default.
- W2135087274 abstract "Intracellular ATP is the most vital source of cellular energy for biologic systems, whereas extracellular ATP is a multifaceted mediator of several cell functions via its interaction, in an autocrine or paracrine manner, with P2 purinergic receptors expressed on the cell surface. These ionotropic and metabotropic P2 purinergic receptors modulate a variety of physiologic events upon the maintenance of a highly sensitive “set point,” the derangement of which may lead to the development of key pathogenic mechanisms during acute and chronic diseases. Growing evidence suggests that extracellular ATP signaling via P2 purinergic receptors may be involved in different renal pathologic conditions. For these reasons, investigators and pharmaceutical companies are actively exploring novel strategies to antagonize or block these receptors with the goal of reducing extracellular ATP production or accelerating extracellular ATP clearance. Targeting extracellular ATP signaling, particularly through the P2X7 receptor, has considerable translational potential, given that novel P2X7-receptor inhibitors are already available for clinical use (e.g., CE224,535, AZD9056, and GSK1482160). This review summarizes the current evidence regarding the involvement of extracellular ATP and its P2 purinergic receptor–mediated signaling in physiologic and pathologic processes in the kidney; potential therapeutic options targeting extracellular ATP purinergic receptors are analyzed as well." @default.
- W2135087274 created "2016-06-24" @default.
- W2135087274 creator A5001694345 @default.
- W2135087274 creator A5028314110 @default.
- W2135087274 creator A5045879499 @default.
- W2135087274 date "2015-05-01" @default.
- W2135087274 modified "2023-10-18" @default.
- W2135087274 title "The Dark Side of Extracellular ATP in Kidney Diseases" @default.
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- W2135087274 doi "https://doi.org/10.1681/asn.2014070721" @default.
- W2135087274 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4413770" @default.
- W2135087274 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25452669" @default.
- W2135087274 hasPublicationYear "2015" @default.
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