Ischemic and non-ischemic preconditioning: Endothelium-focused translation into clinical practice
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Alexander Jabs1, Federica Fasola, Selina Muxel
1Department of Medicine - Cardiology and Angiology, University Medical Center of Mainz, Mainz, Germany.
Insights
Protecting the endothelium from ischemia and reperfusion injury is crucial. Reactive oxygen species (ROS) mediate both damage and protective preconditioning, offering therapeutic targets for cardiovascular conditions.
Area of Science:
- Cardiovascular Pathophysiology
- Endothelial Biology
- Reactive Oxygen Species (ROS) Signaling
Background:
- Endothelial dysfunction is integral to coronary atherosclerosis progression.
- The endothelium is highly susceptible to ischemia and reperfusion injury, influencing tissue damage extent.
- Reactive oxygen species (ROS) are implicated in endothelial risk factor toxicity and reperfusion injury.
Purpose of the Study:
- To explore the bidirectional relationship between endothelial function and ischemia.
- To discuss the role of ROS in endothelial injury and protection.
- To consider pharmacologic strategies for manipulating ROS in endothelial protection.
Main Methods:
- Review of pathophysiological studies on endothelial function and ischemia.
- Discussion of reactive oxygen species' dual role in endothelial damage and preconditioning.
- Considerations presented at the Conference of the European Society of Clinical Hemorheology and Microcirculation.
Main Results:
- Endothelial dysfunction and ischemia have a bidirectional pathophysiological link.
- ROS are key mediators in endothelial injury and reperfusion damage.
- ROS are also critical in mediating endothelial preconditioning, reducing ischemia-reperfusion sensitivity.
Conclusions:
- Protecting the endothelium from ischemia holds significant clinical potential.
- Targeting ROS offers a promising avenue for pharmacologic manipulation of endothelial protection.
- Understanding ROS signaling is vital for managing cardiovascular diseases involving ischemia.
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.
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