Apolipoprotein D, a Novel Ligand for CD36, Is Essential for Blood–Brain Barrier Integrity
Authors' conclusion
Our work identifies a previously unrecognized paracrine mechanism in which mural cell-derived ApoD directly engages endothelial CD36 to restrain pathological endothelial proliferation, thereby preserving BBB integrity and promoting neurological recovery after stroke.
Study context
- Population
- Human brain vs peripheral mural cells; ischemic stroke models (global ApoD knockout, mural cell-specific ApoD knockout, AAV-mediated ApoD overexpression)
Main finding
As reported in the abstract
- Increased ApoD expression in mural cells after ischemic stroke
- Mural cell-derived ApoD acts as inhibitory ligand of endothelial CD36, suppressing pathological endothelial proliferation, preserving blood-brain barrier (BBB) integrity and promoting neurological recovery
- ApoD overexpression in mural cells improved BBB integrity and functional recovery in ApoD-null mice
- ApoD competes with long-chain fatty acids for CD36 binding and attenuates downstream CD36 signaling
- Peripheral hyperglyco-ApoD had minimal effect on BBB integrity; hypoglycosylation enhanced CD36 binding affinity and therapeutic efficacy
- IV hypoglyco-ApoD inhibited BBB disruption and improved neural function, especially in aging stroke
Original publication
Apolipoprotein D, a Novel Ligand for CD36, Is Essential for Blood–Brain Barrier Integrity. Circulation. Published 6 February 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →