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CD36 – A novel molecular target in the neurovascular unit
Abstract
CD36 is an integral membrane protein primarily known for its function as a fatty acid transporter, yet also playing other biological roles from lipid metabolism to inflammation modulation. These pleiotropic effects are explained by the existence of multiple different ligands and the extensive distribution in numerous cell types. Moreover, the receptor is related to various pathologies and it may prove to be a good target for prospective therapeutic strategies. In the neurovascular unit (NVU), CD36 is expressed in cells like microglia, microvascular endothelial cells, astrocytes and neurons. In the normal brain, CD36 was proven to be involved in phagocytosis of apoptotic cells, oro‐sensory detection of dietary lipids, and fatty acid transport across the blood brain barrier (BBB). CD36 was also acknowledged as a potentially important player in central nervous system (CNS) disorders, such as Alzheimer Disease‐associated vascular dysfunction and oxidative stress and the neuroinflammatory response in stroke. Despite continuous efforts, the therapeutic arsenal for such diseases is still scarce and there is an increasing interest in discovering new molecular targets for more specific therapeutic approaches. In this review, we summarize the role of CD36 in the normal function of the NVU and in several CNS disorders, focusing on the dysregulation of the NVU and the potential therapeutic modulation.
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The scavenger receptor family recognizes danger-associated molecular patterns and expression of CD36 mediates cell-specific responses such as inflammatory responses, phagocytosis of apoptotic cells, fatty acid transport across the BBB, and lipid uptake, leading to activation of PPARγ transcriptional pathways.
“The scavenger receptor family recognizes danger‐associated molecular patterns and expression of CD36 mediates cell‐specific responses such as inflammatory responses, phagocytosis of apoptotic cells, fatty acid transport across the BBB, and lipid uptake, leading to activation of PPARγ transcriptional pathways (Canton et al. 2013; Silverstein and Febbraio 2009; Ioghen et al. 2021).”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Ioghen et al. 2021
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Baumart, G. J., Rodrigues, M. S., Sholl, J. N., de Sousa, A. C., Weber, A. F., Costa‐Beber, L. C., Farias, H. R., Costa, M. V., Peres, A. M., de Camargo, P. R., et al. (2026) · Journal of Neurochemistry · doi:10.1111/jnc.70403 · Cited by 2
Metadata
- Authors
- Ioghen, O., Chițoiu, L., Gherghiceanu, M., Ceafalan, L. C., & Hinescu, M. E.
- Affiliations
- Ultrastructural Pathology and Bioimaging Laboratory Victor Babes Institute of Pathology Bucharest Romania
- Department of Cellular and Molecular Biology and Histology School of Medicine Carol Davila Faculty of Medicine Bucharest Romania
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2021-02-28
- Volume
- 53
- Issue
- 8
- Pages
- 2500-2510
- ISSN
- 0953-816X
- 1460-9568
- PMC
- PMC8247892
- Cited by
- 47
- References
- 14
- Language
- en
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