GSK3β Inhibition Ameliorates Atherosclerotic Calcification

Author:

Cai Xinjiang1ORCID,Zhao Yan1,Yang Yang1,Wu Xiuju1ORCID,Zhang Li1ORCID,Ma Jocelyn A.1,Ji Jaden1,Boström Kristina I.12,Yao Yucheng1

Affiliation:

1. Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA

2. The Molecular Biology Institute at UCLA, Los Angeles, CA 90095-1570, USA

Abstract

Endothelial-mesenchymal transition (EndMT) drives endothelium to contribute to atherosclerotic calcification. In a previous study, we showed that glycogen synthase kinase-3β (GSK3β) inhibition induced β-catenin and reduced mothers against DPP homolog 1 (SMAD1) in order to redirect osteoblast-like cells towards endothelial lineage, thereby reducing vascular calcification in Matrix Gla Protein (Mgp) deficiency and diabetic Ins2Akita/wt mice. Here, we report that GSK3β inhibition or endothelial-specific deletion of GSK3β reduces atherosclerotic calcification. We also find that alterations in β-catenin and SMAD1 induced by GSK3β inhibition in the aortas of Apoe−/− mice are similar to Mgp−/− mice. Together, our results suggest that GSK3β inhibition reduces vascular calcification in atherosclerotic lesions through a similar mechanism to that in Mgp−/− mice.

Funder

NIH

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Glycogen synthase kinase 3 activity enhances liver inflammation in MASH;JHEP Reports;2024-06

2. Endothelial Reprogramming in Atherosclerosis;Bioengineering;2024-03-27

3. GSK3 as a Master Regulator of Cellular Processes;International Journal of Molecular Sciences;2023-10-24

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