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Updated: Aug 17, 2026

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
[Cerebral ischemia and apoptosis]
Lorenz Hirt1, Melanie Price, Julien Bogousslavsky
1Service de neurologie, CHUV, 1011 Lausanne. Lorenz.Hirt@chuv.hospvd.ch
Abstract:
Ischemic stroke is an important cause of mortality and invalidity. Focal cerebral ischemia induces multiple and complex mechanisms leading to the loss of function and the demise of cerebral tissue. Apoptosis, or programmed cell death, well known for its role in normal development, is one of these mechanisms, and contributes to ischemic neuronal death. This short review gives an overview of apoptotic mechanisms triggered by cerebral ischemia.
Insights
Ischemic stroke causes death and disability. This review details how programmed cell death (apoptosis) contributes to brain cell death after stroke, impacting neurological function.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Context:
- Ischemic stroke is a leading cause of mortality and long-term disability worldwide.
- Focal cerebral ischemia triggers complex cellular mechanisms contributing to brain tissue damage and functional loss.
Purpose:
- To provide an overview of the apoptotic mechanisms activated by cerebral ischemia.
- To elucidate the role of programmed cell death in ischemic neuronal injury.
Summary:
- Apoptosis, or programmed cell death, is a key mechanism contributing to neuronal demise following ischemic stroke.
- Cerebral ischemia initiates a cascade of events leading to the activation of apoptotic pathways in brain cells.
- Understanding these apoptotic mechanisms is crucial for developing targeted therapeutic strategies.
Impact:
- This review highlights the significance of apoptosis in ischemic stroke pathology.
- Insights into apoptotic pathways may pave the way for novel neuroprotective treatments.
- Reducing apoptosis could mitigate brain damage and improve outcomes for stroke patients.
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