title: The Role of Extracellular Adenosine Triphosphate in Ischemic Organ Injury.
abstract: OBJECTIVE
  Ischemic tissue injury contributes to significant morbidity and mortality and is implicated in a range of pathologic conditions, including but not limited to myocardial infarction, ischemic stroke, and acute kidney injury. The associated reperfusion phase is responsible for the activation of the innate and adaptive immune system, further accentuating inflammation. Adenosine triphosphate molecule has been implicated in various ischemic conditions, including stroke and myocardial infarction.
  
  
  METHODS
  Adenosine triphosphate is a well-defined intracellular energy transfer and is commonly referred to as the body's "energy currency." However, Laboratory studies have demonstrated that extracellular adenosine triphosphate has the ability to initiate inflammation and is therefore referred to as a damage-associated molecular pattern. Purinergic receptors-dependent signaling, proinflammatory cytokine release, increased Ca influx into cells, and subsequent apoptosis have been shown to form a common underlying extracellular adenosine triphosphate molecular mechanism in ischemic organ injury.
  
  
  CONCLUSIONS
  In this review, we aim to discuss the molecular mechanisms behind adenosine triphosphate-mediated ischemic tissue injury and evaluate the role of extracellular adenosine triphosphate in ischemic injury in specific organs, in order to provide a greater understanding of the pathophysiology of this complex process. We also appraise potential future therapeutic strategies to limit damage in various organs, including the heart, brain, kidneys, and lungs.
authors.affiliation: All authors: Anaesthetics, Pain Medicine, and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, United Kingdom.
authors.forename: Hailin
authors.initials: H
authors.lastname: Zhao
authors.forename: Susan
authors.initials: S
authors.lastname: Kilgas
authors.forename: Azeem
authors.initials: A
authors.lastname: Alam
authors.forename: Shiori
authors.initials: S
authors.lastname: Eguchi
authors.forename: Daqing
authors.initials: D
authors.lastname: Ma
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D001921:Brain / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004064:Digestive System / Q000503:physiopathology; D005110:Extracellular Space / Q000378:metabolism*; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D011983:Receptors, Purinergic / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D016207:Cytokines; D011983:Receptors, Purinergic; D000255:Adenosine Triphosphate; D002118:Calcium