The Role of AIF-1 in the Aldosterone-Induced Vascular Calcification Related to Chronic Kidney Disease: Evidence From Mice Model and Cell Co-Culture Model

Increasing evidence suggests that aldosterone (Aldo) plays an essential role in vascular calcification which is a serious threat to cardiovascular disease (CVD) developed from chronic kidney disease (CKD). However, the exact pathogenesis of vascular calcification is still unclear. First, we establis...

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Published in:Frontiers in endocrinology (Lausanne) Vol. 13; p. 917356
Main Authors: Chang, Xueying, Hao, Jianbing, Wang, Xingzhi, Liu, Jingwei, Ni, Jie, Hao, Lirong
Format: Journal Article
Language:English
Published: Frontiers Media S.A 20-07-2022
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Summary:Increasing evidence suggests that aldosterone (Aldo) plays an essential role in vascular calcification which is a serious threat to cardiovascular disease (CVD) developed from chronic kidney disease (CKD). However, the exact pathogenesis of vascular calcification is still unclear. First, we established CKD-associated vascular calcification mice model and knockout mice model to investigate the causal relationship between allograft inflammatory factor 1 (AIF-1) and vascular calcification. Then, endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) co-culture experiments were performed to further explore the mechanisms of calcification. The results of the Aldo intervention mice model and transgenic mice model showed that Aldo could cause calcification by increasing the AIF-1 level. The results of in vitro co-culture model of ECs and VSMCs showed that AIF-1 silence in ECs may alleviate Aldo-induced calcification of VSMCs. In conclusion, our study indicated that Aldo may induce vascular calcification related to chronic renal failure via the AIF-1 pathway which may provide a potential therapeutic target.
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This article was submitted to Renal Endocrinology, a section of the journal Frontiers in Endocrinology
Edited by: Nehal Mohsen Elsherbiny, Mansoura University, Egypt
Reviewed by: James Stewart, University of Mississippi, United States; Mohammad H. Abukhalil, Al-Hussein Bin Talal University, Jordan
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2022.917356