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CD36 as a therapeutic target for endothelial dysfunction in stroke
1Department of Neurology/ Neuroscience, Weill Cornell Medical College at Burke Medical Research Institute, 785 Mamaroneck Ave., White Plains, New York 10605, USA. suc2002@med.cornell.edu
Insights
Stroke involves multiple harmful pathways. Targeting the CD36 receptor and its ligands may offer new therapeutic strategies for stroke by addressing inflammation and endothelial dysfunction.
Area of Science:
- Neuroscience
- Immunology
- Cardiovascular Biology
Background:
- Stroke pathology is complex, involving inflammation, oxidative stress, and cell death pathways.
- Single-pathway interventions have limited success in human stroke due to its multifactorial nature.
- CD36, a scavenger receptor, plays a role in both normal physiology and pathological conditions.
Purpose of the Study:
- To review CD36-ligand interactions relevant to endothelial function.
- To explore the therapeutic potential of targeting CD36 in stroke.
Main Methods:
- Literature review of studies on CD36 pathways and stroke.
- Analysis of CD36's role in inflammation and endothelial dysfunction.
Main Results:
- CD36 activation by various ligands triggers inflammatory responses.
- These responses contribute to endothelial dysfunction, a factor in cardiovascular and cerebrovascular diseases.
- CD36 signaling pathways are implicated in stroke pathology.
Conclusions:
- Targeting CD36 presents a promising therapeutic avenue for stroke.
- Understanding CD36-ligand interactions is crucial for developing effective stroke treatments.
Abstract:
Stroke pathology involves multifactorial pro-death responses, including inflammation, oxidative stress, vascular dysfunction, and activation of necrotic and apoptotic pathways. The interruption of a single specific pathway in defined stroke model systems has not been sufficient to address the multifactorial nature of stroke-induced injuries in the human population. CD36 is a class B scavenger receptor that functions in regulating normal physiological and pathological functions. CD36 pathways are activated by several distinct ligands. Convergence of these pathways results in inflammatory responses and endothelial dysfunction, which may be an underlying cause of cardio- and cerebrovascular diseases. The current review describes receptor CD36-ligand interactions relevant to endothelial function and discusses how targeting CD36 may have therapeutic utility in stroke.
