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

Chang, Xueying; Hao, Jianbing; Wang, Xingzhi; Liu, Jingwei; Ni, Jie; Hao, Lirong

doi:10.3389/fendo.2022.917356

Cited by 7 publications

(6 citation statements)

References 37 publications

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“…VC is a highly regulated process in which calcium-phosphate complexes are deposited in the intima and media and participate in ECs, VSMCs, circulating cells and pro-osteogenic and anti-calcifying factors [93,94]. According to Chang et al, aldosterone induced VC through the AIF1 signaling pathway [32]. By coculturing ECs and VSMCs, we found that aldosterone upregulated AIF1 in ECs, leading to calcium influx and calcification of VSMCs.…”

Section: Kidney Diseasementioning

confidence: 62%

“…By coculturing ECs and VSMCs, we found that aldosterone upregulated AIF1 in ECs, leading to calcium influx and calcification of VSMCs. Additionally, in a mouse model, the aldosterone inhibitor spironolactone downregulated the expression of AIF1, and an AIF1 knockout model of CKD presented attenuated calcification of the aortic wall [32]. Thus, further research on the AIF1-triggered mechanisms in ECs and intercommunication with VSMCs is needed to find proper therapeutic targets that block or reduce VC in CKD patients.…”

Section: Kidney Diseasementioning

confidence: 99%

“…AIF1 is well conserved across the animal kingdom; it has been described in invertebrates [28], including marine sponges [29] and oysters [30]. Several subsequent studies have linked AIF1 with inflammation [31], immunoinflammatory diseases such as kidney disease [32], rheumatoid arthritis [33], cancer [34] or cardiovascular disease [35] and transplant rejection [36]. Moreover, AIF1 may promote macrophage activation and the growth of vascular smooth muscle cells and Tlymphocytes [31,37,38].…”

Section: Introductionmentioning

confidence: 99%

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AIF1: Function and Connection with Inflammatory Diseases

De Leon-Oliva,

Garcia-Montero,

Fraile-Martinez

et al. 2023

Biology

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Macrophages are a type of immune cell distributed throughout all tissues of an organism. Allograft inflammatory factor 1 (AIF1) is a calcium-binding protein linked to the activation of macrophages. AIF1 is a key intracellular signaling molecule that participates in phagocytosis, membrane ruffling and F-actin polymerization. Moreover, it has several cell type-specific functions. AIF1 plays important roles in the development of several diseases: kidney disease, rheumatoid arthritis, cancer, cardiovascular diseases, metabolic diseases and neurological disorders, and in transplants. In this review, we present a comprehensive review of the known structure, functions and role of AIF1 in inflammatory diseases.

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Section: Kidney Diseasementioning

confidence: 62%

Section: Kidney Diseasementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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AIF1: Function and Connection with Inflammatory Diseases

De Leon-Oliva,

Garcia-Montero,

Fraile-Martinez

et al. 2023

Biology

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“…The serum AIF1 concentration was independently correlated with the logarithm of urinary albumin excretion ( β = 0.213, P = 0.0120) and with the eGFR ( β = − 0.286, P = 0.0011) [ 58 ]. Mechanistically, aldosterone may induce vascular calcification related to chronic renal failure via the AIF1 pathway [ 59 ]. In addition, our SMR analysis with GTEx data for 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2) was also consistent with a longitudinal data analysis in American Indians, which reported that the variation in PFKFB2 appears to reduce PFKFB2 expression in adipose and kidney tissues and thereby increase the risk for adiposity and diabetic nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Identification of novel therapeutic targets for chronic kidney disease and kidney function by integrating multi-omics proteome with transcriptome

Si,

Liu,

et al. 2024

Genome Med

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Background Chronic kidney disease (CKD) is a progressive disease for which there is no effective cure. We aimed to identify potential drug targets for CKD and kidney function by integrating plasma proteome and transcriptome. Methods We designed a comprehensive analysis pipeline involving two-sample Mendelian randomization (MR) (for proteins), summary-based MR (SMR) (for mRNA), and colocalization (for coding genes) to identify potential multi-omics biomarkers for CKD and combined the protein–protein interaction, Gene Ontology (GO), and single-cell annotation to explore the potential biological roles. The outcomes included CKD, extensive kidney function phenotypes, and different CKD clinical types (IgA nephropathy, chronic glomerulonephritis, chronic tubulointerstitial nephritis, membranous nephropathy, nephrotic syndrome, and diabetic nephropathy). Results Leveraging pQTLs of 3032 proteins from 3 large-scale GWASs and corresponding blood- and tissue-specific eQTLs, we identified 32 proteins associated with CKD, which were validated across diverse CKD datasets, kidney function indicators, and clinical types. Notably, 12 proteins with prior MR support, including fibroblast growth factor 5 (FGF5), isopentenyl-diphosphate delta-isomerase 2 (IDI2), inhibin beta C chain (INHBC), butyrophilin subfamily 3 member A2 (BTN3A2), BTN3A3, uromodulin (UMOD), complement component 4A (C4a), C4b, centrosomal protein of 170 kDa (CEP170), serologically defined colon cancer antigen 8 (SDCCAG8), MHC class I polypeptide-related sequence B (MICB), and liver-expressed antimicrobial peptide 2 (LEAP2), were confirmed. To our knowledge, 20 novel causal proteins have not been previously reported. Five novel proteins, namely, GCKR (OR 1.17, 95% CI 1.10–1.24), IGFBP-5 (OR 0.43, 95% CI 0.29–0.62), sRAGE (OR 1.14, 95% CI 1.07–1.22), GNPTG (OR 0.90, 95% CI 0.86–0.95), and YOD1 (OR 1.39, 95% CI 1.18–1.64,) passed the MR, SMR, and colocalization analysis. The other 15 proteins were also candidate targets (GATM, AIF1L, DQA2, PFKFB2, NFATC1, activin AC, Apo A-IV, MFAP4, DJC10, C2CD2L, TCEA2, HLA-E, PLD3, AIF1, and GMPR1). These proteins interact with each other, and their coding genes were mainly enrichment in immunity-related pathways or presented specificity across tissues, kidney-related tissue cells, and kidney single cells. Conclusions Our integrated analysis of plasma proteome and transcriptome data identifies 32 potential therapeutic targets for CKD, kidney function, and specific CKD clinical types, offering potential targets for the development of novel immunotherapies, combination therapies, or targeted interventions.

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“…Approximately 40% of patients with end-stage renal disease (ESRD) die due to CVD. ESRD patients have complications of CVD, and these complications usually have a strong association with VC [ 13 ]. VC is one manifestation of arteriosclerosis but not atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Panax notoginseng Suppresses Bone Morphogenetic Protein-2 Expression in EA.hy926 Endothelial Cells by Inhibiting the Noncanonical NF-κB and Wnt/β-Catenin Signaling Pathways

Ping

Hsieh

Wang

et al. 2022

Plants

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Panax notoginseng (PN) exerts cardiovascular-disease-protective effects, but the effect of PN on reducing vascular calcification (VC) is unknown. Under the VC process, however, endothelial bone morphogenetic protein-2 (BMP-2) signals connect endothelial and smooth muscle cells. To investigate the effects of PN water extract (PNWE) on BMP-2 expression, human EA.hy926 endothelial cells were pretreated with PNWE for 48 h, and BMP-2 expression was then induced using warfarin/β-glycerophosphate (W/BGP) for another 24 h. The expression of BMP-2, the degrees of oxidative stress and inflammation, and the activation of noncanonical NF-κB and Wnt/β-catenin signaling were analyzed. The results showed that the BMP-2 levels in EA.hy926 cells were reduced in the groups treated with 10, 50, or 100 μg/mL PNWE combined with W/BGP. PNWE combined with W/BGP significantly reduced thiobarbituric-acid-reactive substrate and reactive oxygen species levels as well as prostaglandin E2, IL-1β, IL-6, and TNF-α. PNWE (10, 50, and 100 μg/mL) reduced the p52 levels and p52/p100 protein ratio. Wnt and β-catenin protein expression was decreased in the groups treated with PNWE combined with W/BGP. These results showed that PNWE reduced BMP-2 expression in EA.hy926 cells by inhibiting the noncanonical NF-κB and Wnt/β-catenin signaling pathways.

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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

Cited by 7 publications

References 37 publications

AIF1: Function and Connection with Inflammatory Diseases

AIF1: Function and Connection with Inflammatory Diseases

Identification of novel therapeutic targets for chronic kidney disease and kidney function by integrating multi-omics proteome with transcriptome

Panax notoginseng Suppresses Bone Morphogenetic Protein-2 Expression in EA.hy926 Endothelial Cells by Inhibiting the Noncanonical NF-κB and Wnt/β-Catenin Signaling Pathways

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