Hypotaurine reduces glucose-mediated vascular calcification
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ABSTRACT:
PROVIDER: PRJNA1195053 | ENA |
REPOSITORIES: ENA
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Project description:To study the underlying molecular mechanisms driving vascular calcification, we analyzed the transcriptome of calcium-phosphate calcified human coronary aortic smooth muscle cells cultured with zero, low, and high glucose for 3 days.
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Project description:Vascular calcification is the major risk factor for increased cardiovascular morbidity and mortality in patients with CKD, especially those with advanced renal diseases. However, once mineral deposits form in vascular tissue, no specific therapies can completely arrest or reverse the progression of calcification. Here, we identified that decreased serum soluble αKlotho levels are characteristic events in the development of vascular calcification in patients with early CKD. We employed a transcriptomicsapproach, as well as in vitro and in vivo vascular calcification models, and determined that soluble αKlotho specifically suppressed Hsp90aa1 activation-mediated osteogenic transdifferentiation of VSMCs and vascular calcification. Moreover, we revealed that the phosphorylation of Hsp90aa1 at Thr5/7 modulated its chaperone activity to stabilize Hif1α, thereby playing a causative role in the pathogenesis of vascular calcification in response to CKD. Upregulation of soluble αKlotho expression in VSMCs enhanced the interaction with Hsp90aa1, which abolished Hsp90aa1-Hif1α axis activation in response to osteogenic induction. Together, these results identify a key pathway in VSMCs that mediates vascular calcification, which could be used as a potential therapeutic target.
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Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC. Calcification was induced in rat aorta vascular smooth muscle cells with inorganic phosphate (Pi). Total RNA were extracted from the cells 3 and 6 days later. mRNA profile of the sample was compared with normal control.
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Project description:Vascular calcification contributes to the cardiovascular morbidity and mortality of chronic kidney disease (CKD), but there is no approved treatment for vascular calcification. In this study, we report the role of STING in vascular calcification. To further investigate the molecular mechanism by which STING participates in vascular calcification, we performed high-throughput RNA-seq to identify the target gene of STING.
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Project description:Vascular calcification, a key risk factor for cardiovascular diseases, is driven by the phenotypic transition of vascular smooth muscle cells (VSMCs) from a contractile to an osteogenic phenotype. NEXN, a protein highly associated with heart function, has also been implicated as a potential susceptibility factor in the development of coronary artery disease, but its role in the progression of vascular calcification remains unclear. In this study, multi-transcriptomics analysis and various animal models were used to explore the cell-specific roles and molecular mechanisms of NEXN in vascular calcification. VSMC-specific NEXN knockout exacerbated calcification, while NEXN overexpression alleviated it. NEXN was shown to interact with SERCA2, enhancing its SUMOylation, stability, and function, thereby protecting against calcification. These findings suggest that NEXN modulates vascular calcification through SERCA2 stabilization, offering potential therapeutic strategies by targeting NEXN-SERCA2 interactions or enhancing SERCA2 SUMOylation to prevent vascular calcification and its complications.
2025-06-04 | GSE297578 | GEO
Project description:Vascular calcification is the abnormal deposition of calcium phosphates within the blood vessels. Although it significantly contributes to the development of cardiovascular disease, much remains unknown about the mechanisms driving this process. Recent advances have shown that microRNAs (miRNAs) could be critical in regulating the biological processes driving vascular calcification. Here, we investigated whether miR-26b could regulate vascular calcification. By performing bulk RNA-seq of the aorta of miR-26bKO mice, we identified cell-specific targets and demonstrated that BMP signalling is dysregulated in aortic cells.
2025-11-14 | GSE281279 | GEO
Project description:Vascular calcification is the abnormal deposition of calcium phosphates within the blood vessels. Although it significantly contributes to the development of cardiovascular disease, much remains unknown about the mechanisms driving this process. Recent advances have shown that microRNAs (miRNAs) could be critical in regulating the biological processes driving vascular calcification. Here, we investigated whether miRNA-26b (miR-26b) could regulate vascular calcification. By performing scRNA-seq of the aorta of miR-26b knockout (miR-26bKO) mice, we identified cell-specific targets and demonstrated that components of the BMP signalling pathway are dysregulated in the aortic cell types.
2025-11-14 | GSE281028 | GEO
Project description:In this study, we report the protective effect of LINE1 intervention on vascular calcification. To elucidate the molecular mechanisms underlying the protective role of LINE1 inhibition, we employed RNA sequencing to identify gene expression changes under LINE1 suppression conditions. Our findings provide insights into the pathways involved in modulating vascular calcification and highlight LINE1 as a potential therapeutic target.
2025-07-15 | GSE279148 | GEO
Project description:In this study, we report the protective effect of β-hydroxybutyrate (BHB) on vascular calcification in chronic kidney disease (CKD). To further investigate the mechanism underpinning the protective effect of BHB on vascular calcification, we performed high-throughput RNA-seq to identify the target gene of BHB. Our data demonstrate that BHB supplementation inhibits vascular calcification in CKD via targeting HDAC9.
2021-11-01 | GSE186772 | GEO
Project description:Objective: To investigate the treatment and mechanism of lanthanum hydroxide on hyperphosphate-induced vascular calcification in chronic renal failure. Methods: Develop a rat model of CKD hyperphosphatemia. Rats were randomly allocated to the model, lanthanum hydroxide, lanthanum carbonate, Calcium carbonate groups. Determination of serum biochemical indicators and the determination of pathological analysis of kidney tissue, Von Kossa staining and CT scan on the aortic vessels. The proteomic analysis of aortic tissue in Vivo. A calcified VSMCs model was established. The calcium content and ALP activity were measured. RT-PCR measures the mRNA expression level of SM22α, Runx2, BMP-2 and TRAF6. Western Blot measures the protein expression level of SM22α, Runx2, BMP-2, TRAF6 and NF-κB. Results: Through the detection of serum biochemical indicators and pathological analysis of kidney tissue, it can be summaryed that lanthanum hydroxide has the effect of delaying the progression of renal failure and protecting renal function. We found that the administration of lanthanum hydroxide delayed the development of vascular calcification induced by hyperphosphatemia in CKD. It can be concluded that lanthanum hydroxide may affect vascular calcification through the NF-κB pathway. , To deal with Lanthanum chloride (LaCl3) inhibited phosphate induced calcification, osteo-/chondrogenic transdifferentiation, and NF-κB signaling in cultured VSMCs. Lanthanum hydroxide significantly reduces the expression of Runx2, BMP-2, TRAF6 and NF-κB. Conclusion: Lanthanum hydroxide has a protective effect on the kidneys, and can delay the development of vascular calcification by reducing serum phosphorus concentration.
2021-09-09 | PXD023081 | Pride