title: Ischemic and non-ischemic preconditioning: Endothelium-focused translation into clinical practice.
abstract: Pathophysiological studies have clearly demonstrated that the relationship between endothelial [dys]function and tissue ischemia is bidirectional: while it is well accepted that endothelial dysfunction has a key role in the progression and destabilization of coronary atherosclerosis, it is also well known that the endothelium is particularly sensitive to ischemia and reperfusion injury, and that this damage critically determines the extent of tissue damage, e.g. myocardial infarct size. Therefore, protecting the endothelium from ischemia could potentially have important clinical implications. In this scenario, reactive oxygen species [ROS] play a particularly important role: these elusive mediators are involved in determining the endothelial toxic effect of risk factors and are involved in reperfusion injury; however, most importantly, ROS are also key mediators of endothelial preconditioning, a protective process that is characterized by a reduced sensitivity to ischemia and reperfusion injury. We report considerations regarding these phenomena and their potential pharmacologic manipulation as discussed in a lecture at the recent Conference of the European Society of Clinical Hemorheology and Microcirculation held in Pontresina, Switzerland.
authors.affiliation: Department of Medicine - Cardiology and Angiology, University Medical Center of Mainz, Mainz, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Jabs
authors.forename: Federica
authors.initials: F
authors.lastname: Fasola
authors.forename: Selina
authors.initials: S
authors.lastname: Muxel
authors.forename: Thomas
authors.initials: T
authors.lastname: Münzel
authors.forename: Tommaso
authors.initials: T
authors.lastname: Gori
mesh_terms: D004730:Endothelium, Vascular / Q000473:pathology*; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D017202:Myocardial Ischemia / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors
chemical_list: D017382:Reactive Oxygen Species