Loss of the heterogeneous expression of flippase ATP11B leads to cerebral small vessel disease in a normotensive rat model.

ABSTRACT: Cerebral small vessel disease (SVD) is the leading cause of vascular dementia, causes a quarter of strokes, and worsens stroke outcomes. The disease is characterised by patchy cerebral small vessel and white matter pathology, but the underlying mechanisms are poorly understood. This microvascular and tissue damage has been classically considered secondary to extrinsic factors, such as hypertension, but this fails to explain the patchy nature of the disease, the link to endothelial cell (EC) dysfunction even when hypertension is absent, and the increasing evidence of high heritability to SVD-related brain damage. We have previously shown the link between deletion of the phospholipase flippase Atp11b and EC dysfunction in an inbred hypertensive rat model with SVD-like pathology and a single

SUBMITTER: Quick S 

PROVIDER: S-EPMC9288385 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature