title: Beneficial and detrimental role of adenosine signaling in diseases and therapy.
abstract: Adenosine is a major signaling nucleoside that orchestrates cellular and tissue adaptation under energy depletion and ischemic/hypoxic conditions by activation of four G protein-coupled receptors (GPCR). The regulation and generation of extracellular adenosine in response to stress are critical in tissue protection. Both mouse and human studies reported that extracellular adenosine signaling plays a beneficial role during acute states. However, prolonged excess extracellular adenosine is detrimental and contributes to the development and progression of various chronic diseases. In recent years, substantial progress has been made to understand the role of adenosine signaling in different conditions and to clarify its significance during the course of disease progression in various organs. These efforts have and will identify potential therapeutic possibilities for protection of tissue injury at acute stage by upregulation of adenosine signaling or attenuation of chronic disease progression by downregulation of adenosine signaling. This review is to summarize current progress and the importance of adenosine signaling in different disease stages and its potential therapeutic effects.
authors: Department of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston, Houston, Texas; Graduate School of Biomedical Science, University of Texas Health Science Center at Houston, Houston, Texas; Department of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China; and.
authors: Hong
authors: H
authors: Liu
authors: Department of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston, Houston, Texas; Graduate School of Biomedical Science, University of Texas Health Science Center at Houston, Houston, Texas; Department of Nephrology, Xiangya Hospital, Central South University, Changsha, Hunan, China yang.xia@uth.tmc.edu.
authors: Yang
authors: Y
authors: Xia
mesh_terms: D000241:Adenosine / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000378:metabolism; D002908:Chronic Disease / Q000628:therapy*; D006801:Humans; D058906:Purinergic P1 Receptor Agonists / Q000494:pharmacology / Q000627:therapeutic use; D058915:Purinergic P1 Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D018047:Receptors, Purinergic P1 / Q000378:metabolism*; D012120:Respiration Disorders / Q000188:drug therapy / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
chemical_list: D058906:Purinergic P1 Receptor Agonists; D058915:Purinergic P1 Receptor Antagonists; D043562:Receptors, G-Protein-Coupled; D018047:Receptors, Purinergic P1; D000241:Adenosine
keywords: adenosine signaling; disease; hypoxia; therapy