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.

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.
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AIF-1 在醛固酮诱导的慢性肾病血管钙化中的作用:来自小鼠模型和细胞共培养模型的证据

DOI:
10.3389/fendo.2022.917356
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发表时间:
2022
影响因子:
5.2
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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越来越多的证据表明,醛固酮 (Aldo) 在血管钙化中发挥重要作用,血管钙化对慢性肾病 (CKD) 引起的心血管疾病 (CVD) 构成严重威胁。然而,血管钙化的确切发病机制仍不清楚。首先,我们建立了CKD相关血管钙化小鼠模型和基因敲除小鼠模型,以探讨同种异体移植物炎症因子1(AIF-1)与血管钙化之间的因果关系。然后,进行内皮细胞(EC)和血管平滑肌细胞(VSMC)共培养实验,以进一步探讨钙化的机制。 Aldo干预小鼠模型和转基因小鼠模型的结果表明,Aldo可以通过增加AIF-1水平引起钙化。 ECs和VSMCs体外共培养模型的结果表明,ECs中AIF-1的沉默可以减轻Aldo诱导的VSMCs钙化。总之,我们的研究表明 Aldo 可能通过 AIF-1 途径诱导与慢性肾衰竭相关的血管钙化,这可能提供潜在的治疗靶点。
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.
DOI: 10.1016/j.cellsig.2018.04.004
发表时间: 2018-07
影响因子: 4.8
作者:
Harper E;Rochfort KD;Forde H;Davenport C;Smith D;Cummins PM
通讯作者: Cummins PM