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The Role of CD36 in Stroke-Induced Inflammation and Brain Injury

RESEARCH PROJECT: 
In Progress

Despite a well-documented role of CD36 in the pathogenesis of conditions such as atherosclerosis, inflammation and lipid metabolism, its role in cerebral ischemic injury had not been recognized at the time I initiated the study on CD36. Our report on CD36 was the first study to demonstrate the role of this receptor in inflammation and brain injury following ischemic stroke. Since CD36 is expressed in many different tissues and cell types, including peripheral monocytes/macrophages, my study also focused on the effect of CD36 expressed in the peripheral organs including bone marrow, spleen and blood. The major findings from these studies are the recognition of peripheral immunity on CNS injury, validating CD36 as a target in acute pathology, and characterizing a pharmacological agent that inhibits CD36 pathways. These studies made a major contribution toward identifying novel molecular targets that may serve as possible therapeutic strategies to attenuate acute stroke pathology.

Funding

GRANT: 
Federal
September 30, 2015 to August 31, 2021
Funding Status: 
Completed Project
National Institutes of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Grant Number: 
R01NS095359
Investigators: 
Principal Investigator
GRANT: 
Federal
February 15, 2006 to June 30, 2015
Funding Status: 
Completed Project
National Institutes of Health (NIH)
National Heart Lung and Blood Institute (NHLBI)
Grant Number: 
R01HL082511
Investigators: 
Principal Investigator

Associated

Conditions & Recovery

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Stroke is the leading cause of disability in the U.S.
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Write and walk again.

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