Accelerated atherosclerosis development in C57Bl6 mice by overexpressing AAV-mediated PCSK9 and partial carotid ligation - Laboratory Investigation
![Accelerated atherosclerosis development in C57Bl6 mice by overexpressing AAV-mediated PCSK9 and partial carotid ligation - Laboratory Investigation](https://www.laboratoryinvestigation.org/cms/attachment/0008d7a2-edbc-4b53-a4ec-0ecc04ca922f/gr6.jpg)
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Experimental design. Partial ligation of the LCCA in ApoE-/- mice at
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Frontiers Protein Phosphatase 2A Deficiency in Macrophages Increases Foam Cell Formation and Accelerates Atherosclerotic Lesion Development
![](https://www.researchgate.net/publication/281623624/figure/fig1/AS:614175147556865@1523442174487/Mechanism-of-action-and-clearance-for-PCSK9-and-anti-PCSK9-antibodies-Notes-A.png)
Mechanism of action and clearance for PCSK9 and anti-PCSK9 antibodies.
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Diet-induced hepatic steatosis abrogates cell-surface LDLR by inducing de novo PCSK9 expression in mice - Journal of Biological Chemistry
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Partial carotid ligation is a model of acutely induced disturbed flow, leading to rapid endothelial dysfunction and atherosclerosis
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Somatic Editing of Ldlr With Adeno-Associated Viral-CRISPR Is an Efficient Tool for Atherosclerosis Research
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Advancing age increases the size and severity of spontaneous atheromas in mouse models of atherosclerosis
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Targeting mechanosensitive endothelial TXNDC5 to stabilize eNOS and reduce atherosclerosis in vivo
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Induction of Sustained Hypercholesterolemia by Single Adeno-Associated Virus–Mediated Gene Transfer of Mutant hPCSK9
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Pla2g12b is Essential for Expansion of Nascent Lipoprotein Particles