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Cell Death Pathways in Ischemic Stroke and Targeted Pharmacotherapy
Aishika Datta1, Deepaneeta Sarmah1, Leela Mounica1
1Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Gandhinagar, Gujarat, 382355, India.
Translational Stroke Research
|March 29, 2020
Summary
Ischemic stroke causes significant cell injury, with reperfusion worsening damage. Understanding diverse cell death pathways, including apoptosis, is key to developing new treatments for protecting salvageable neurons.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Ischemic stroke is a leading cause of death and disability worldwide.
- Cellular injury and death in the infarct zone are critical consequences of focal cerebral ischemia.
- Reperfusion following ischemia can paradoxically worsen tissue damage and increase infarct size.
Purpose of the Study:
- To explore the mechanisms of cell death following ischemic stroke.
- To differentiate between regulated and non-regulated cell death pathways in the context of cerebral ischemia.
- To highlight the importance of understanding these pathways for developing novel therapeutic strategies.
Main Methods:
- Review of classical and non-classical cell death pathways.
- Analysis of cellular injury mechanisms in ischemic stroke models.
- Investigation of signaling cascades and effector mechanisms in cell death.
Main Results:
- Cellular injuries in ischemic stroke follow both regulated (e.g., apoptosis) and non-regulated (accidental) pathways.
- Non-classical, non-apoptotic regulated cell death pathways are increasingly recognized.
- Ischemic penumbral neurons, while dysfunctional, remain potentially salvageable.
Conclusions:
- Understanding the diverse cell death pathways in ischemic stroke is crucial for therapeutic development.
- Targeting specific cell death mechanisms, particularly apoptosis, may offer new treatment avenues.
- Protecting salvageable neurons in the ischemic penumbra is a primary goal for stroke treatment.
