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Ionic regulation of cell volume changes and cell death after ischemic stroke
1Department of Anesthesiology, Emory University School of Medicine, 101 Woodruff Circle, WMB Building Suite 620, Atlanta, GA, 30322, USA.
Translational Stroke Research
|December 11, 2013
Summary
Stroke-induced cell swelling and shrinkage involve ion channel and transporter dysfunction. Na+/K+-ATPase failure disrupts ionic homeostasis, leading to cell death and offering targets for stroke research.
Area of Science:
- Neuroscience
- Cell Biology
- Pathophysiology
Background:
- Stroke is a major cause of death and disability globally.
- Early ischemic events trigger cytotoxic cell swelling via ion influx.
- Later stages involve cell shrinkage linked to programmed cell death.
Purpose of the Study:
- To review the regulation of pathological cell volume changes post-ischemia.
- To highlight the role of ion channels, receptors, and energy metabolism.
- To introduce the concept of hybrid cell death in ischemic conditions.
Main Methods:
- Literature review of research on ischemic cell volume regulation.
- Analysis of ion channels (NMDA, AMPA, ASIC, TRP, KCNQ) and hemichannels.
- Examination of Na+/K+-ATPase function and energy deficiency.
Main Results:
- Pathological cell volume changes are regulated by specific ion channels and receptors.
- Energy deficiency and Na+/K+-ATPase dysfunction are critical in ischemia.
- Na+ pump failure precedes ionic homeostasis disruption and cell death.
Conclusions:
- Understanding ionic mechanisms of ischemic cytotoxicity is advancing.
- Na+/K+-ATPase failure is a key event in ischemic cell death.
- Targeting these ionic pathways may offer novel therapeutic strategies for stroke.
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