Why the study?
Aldosterone plays an essential role in vascular calcification related to chronic kidney disease, but the exact pathogenesis remains unclear.
Aldosterone induces vascular calcification in chronic kidney disease via the AIF-1 pathway, suggesting AIF-1 as a potential therapeutic target.
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AIF-1 may mediate vascular calcification in CKD animal models; leaves open its human relevance and requires prospective validation.
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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Chang et al. (2022) studied this question.
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