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CD36: a multi-modal target for acute stroke therapy
1Burke/Cornell Medical Research Institute, White Plains, New York, New York 10605, USA. suc2002@med.cornell.edu
Insights
CD36, a known inflammatory receptor, plays a significant role in cerebral ischemia pathogenesis. Targeting CD36 offers a promising therapeutic strategy for stroke, especially in patients with hyperlipidemia and diabetes.
Area of Science:
- Neuroscience
- Immunology
- Cardiovascular Research
Background:
- CD36 is implicated in atherosclerosis, inflammation, and lipid metabolism.
- Its role in cerebral ischemia remains largely unexplored.
- CD36 functions as a prototypic inflammatory receptor.
Purpose of the Study:
- To establish CD36 as a key contributor to cerebral ischemia pathogenesis.
- To highlight CD36 as a potential therapeutic target for stroke.
- To explore the influence of hyperlipidemia and diabetes on CD36-mediated stroke.
Main Methods:
- Review of existing literature on CD36 functions.
- Analysis of CD36's role in experimental models of cerebral ischemia.
- Focus on risk factors like hyperlipidemia and diabetes.
Main Results:
- CD36 contributes to the pathogenesis of cerebral ischemia.
- Clinical trial failures may stem from inadequate animal models.
- Hyperlipidemia and diabetes modulate CD36 responses in stroke.
Conclusions:
- Blocking CD36 offers a novel therapeutic strategy for stroke.
- Clinically relevant models are crucial for translational studies.
- Understanding CD36's role can lead to effective treatments for stroke victims.
Abstract:
A role for CD36 in the pathogenesis of atherosclerosis, inflammation and lipid metabolism has been well-documented. However, little is known about the role of CD36 in cerebral ischemia. The intent of this review is to develop the concept that CD36, whose functions have been implicated in other pathological events, is a prototypic inflammatory receptor that contributes to the pathogenesis of cerebral ischemia. The importance of CD36 as a treatment target is indicated by the fact that many treatment strategies that are effective in experimental models of stroke exhibit little or no efficacy in clinical trials. The failure of clinical trials may be due to the use of animal models of stroke that do not reflect traditional risk factors for stroke in humans. The discussion will be focused on two risk factors, hyperlipidemia and diabetes, that modulate CD36 responses. Blocking the expression and function of CD36 by pharmacological or genetic means will provide insight not only toward identifying CD36 as a novel molecular target but also for developing effective therapeutic strategies to treat stroke victims. More importantly, coupling clinically relevant conditions with CD36-mediated ischemic injury may provide an appropriate animal model paradigm and develop a scientific understanding that could lead to clinical translational studies involving human subjects.
