Gene inactivation of lysyl oxidase in smooth muscle cells reduces atherosclerosis burden and plaque calcification in hyperlipidemic mice.

ABSTRACT:

Background and aims

Lysyl oxidase (LOX) catalyzes the crosslinking of collagen and elastin to maintain tensile strength and structural integrity of the vasculature. Excessive LOX activity increases vascular stiffness and the severity of occlusive diseases. Herein, we investigated the mechanisms by which LOX controls atherogenesis and osteogenic differentiation of vascular smooth muscle cells (SMC) in hyperlipidemic mice.

Methods

Gene inactivation of Lox in SMC was achieved in conditional knockout mice after tamoxifen injections. Atherosclerosis burden and vascular calcification were assessed in hyperlipidemic conditional [Lox^f/fMyh11-CreER^T2ApoE^-/-] and sibling control mice [Lox^wt/wtMyh11-CreER^T2ApoE^-/-]. Mech

SUBMITTER: Stoyell-Conti FF 

PROVIDER: S-EPMC11465391 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature