Smooth muscle-specific deletion of cellular communication network factor 2 causes severe aorta malformation and atherosclerosis.

ABSTRACT:

Aims

Cellular communication network factor 2 (CCN2) is a matricellular protein implicated in fibrotic diseases, with ongoing clinical trials evaluating anti-CCN2-based therapies. By uncovering CCN2 as abundantly expressed in non-diseased artery tissue, this study aimed to investigate the hypothesis that CCN2 plays a pivotal role in maintaining smooth muscle cell (SMC) phenotype and protection against atherosclerosis.

Methods and results

Global- and SMC-specific Ccn2 knockout mouse models were employed to demonstrate that Ccn2 deficiency leads to SMC de-differentiation, medial thickening, and aorta elongation under normolipidaemic conditions. Inducing hyperlipidaemia in both models resulted in severe aorta malformation and a 17-fold increase in atherosclerosis formation. Lipi

SUBMITTER: Larsen JH 

PROVIDER: S-EPMC11630017 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature