Key result
NRP2 knockdown mitigated low shear stress-induced endothelial cell apoptosis and the development of atherosclerosis in Apoe -/- mice by regulating PARP1 expression.
Why the study?
Endothelial dysfunction caused by disturbed flow is an early step in atherosclerosis, but the mechanism regulating Neuropilin 2 under low shear stress in the atheroprone endothelial phenotype is not well understood.
Population
LSS-stimulated HUVECs, mouse aortic endothelial cells, and Apoe–/– mice
Comparison
NRP2 knockdown or overexpression vs control conditions
Design
Preclinical in vitro and in vivo mechanistic study
Authors
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NRP2 inhibition merits exploration as atherosclerosis therapy; animal data leave open translation to human patients.
NRP2 promotes atherosclerosis by upregulating PARP1 and enhancing endothelial cell apoptosis under low shear stress, identifying it as a potential therapeutic target for atherosclerotic disorders.
Wang et al. (2022) studied Atherosclerosis. NRP2 knockdown vs. Control was evaluated on Cell apoptosis and development of atherosclerosis. NRP2 knockdown mitigated low shear stress-induced endothelial cell apoptosis and the development of atherosclerosis in Apoe -/- mice by regulating PARP1 expression.
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