title: Pharmacology of Ischemia-Reperfusion. Translational Research Considerations.
abstract: Ischemia-reperfusion (IRI) is a complex physiopathological mechanism involving a large number of metabolic processes that can eventually lead to cell apoptosis and ultimately tissue necrosis. Treatment approaches intended to reduce or palliate the effects of IRI are varied, and are aimed basically at: inhibiting cell apoptosis and the complement system in the inflammatory process deriving from IRI, modulating calcium levels, maintaining mitochondrial membrane integrity, reducing the oxidative effects of IRI and levels of inflammatory cytokines, or minimizing the action of macrophages, neutrophils, and other cell types. This study involved an extensive, up-to-date review of the bibliography on the currently most widely used active products in the treatment and prevention of IRI, and their mechanisms of action, in an aim to obtain an overview of current and potential future treatments for this pathological process. The importance of IRI is clearly reflected by the large number of studies published year after year, and by the variety of pathophysiological processes involved in this major vascular problem. A quick study of the evolution of IRI-related publications in PubMed shows that in a single month in 2014, 263 articles were published, compared to 806 articles in the entire 1990.
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: Beatriz
authors.initials: B
authors.lastname: Prieto-Moure
authors.affiliation: a Department of Surgery , University of Valencia , Valencia , Spain.
authors.forename: José M
authors.initials: JM
authors.lastname: Lloris-Carsí
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: Carlos
authors.initials: C
authors.lastname: Barrios-Pitarque
authors.affiliation: c Western Michigan University, Homer Stryker M.D. School of Medicine and Michigan State University , College of Human Medicine , Kalamazoo , MI.
authors.forename: Luis-H
authors.initials: LH
authors.lastname: Toledo-Pereyra
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: José María
authors.initials: JM
authors.lastname: Lajara-Romance
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: M
authors.initials: M
authors.lastname: Berda-Antolí
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: J M
authors.initials: JM
authors.lastname: Lloris-Cejalvo
authors.affiliation: b Experimental Surgery , Catholic University of Valencia , Valencia , Spain.
authors.forename: Dolores
authors.initials: D
authors.lastname: Cejalvo-Lapeña
mesh_terms: D018685:Anesthetics, Inhalation / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D003165:Complement System Proteins / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D019194:Ischemic Preconditioning / Q000379:methods*; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D053610:Opiate Alkaloids / Q000627:therapeutic use; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D057170:Translational Research, Biomedical / Q000639:trends*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D018685:Anesthetics, Inhalation; D000975:Antioxidants; D016207:Cytokines; D018836:Inflammation Mediators; D016328:NF-kappa B; D053610:Opiate Alkaloids; D014409:Tumor Necrosis Factor-alpha; D003165:Complement System Proteins
keywords: antioxidants; ischemia-reperfusion; macrophage/neutrophil reduction; more common therapies; pharmacology; preconditioning; reduction of inflammatory cytokines