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Valvular lipidomic changes in progression of human calcific aortic valve stenosis

ABSTRACT: This study investigates lipid dysregulation in calcific aortic valve stenosis (CAVS) by analyzing lipid profiles in valve tissues from 99 patients across different disease severities (mild, moderate, severe) using liquid chromatography-mass spectrometry (LC-MS). The results reveal distinct lipid alterations that correspond to disease progression, with significant correlations between diacylglycerol (DG) and alkyl lysophosphatidylcholine (LPC(O)) levels and key markers of valve stiffness, such as peak aortic jet velocity and mean pressure gradient. Unique lipid profiles, marked by elevated cholesteryl esters and triacylglycerols, were identified in fast-progressing cases. Additionally, plasma lipids TG 52:4 and TG 54:4 emerged as promising non-invasive diagnostic markers, surpassing traditional markers in diagnostic performance. This study highlights the potential of specific lipidomic pathways as therapeutic targets in CAVS, given the current lack of effective pharmacological treatments.

INSTRUMENT(S): Liquid Chromatography MS -, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS11713 | MetaboLights | 2025-01-28

REPOSITORIES: MetaboLights

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			Action	DRS
	Batch1_Plasma_MRM1_Aug28_2020.wiff	Wiff
	Batch1_Plasma_MRM1_Aug28_2020.wiff.scan	Wiff
	Batch1_Plasma_MRM2_Aug29_2020.wiff	Wiff
	Batch1_Plasma_MRM2_Aug29_2020.wiff.scan	Wiff
	Batch1_Tissue_MRM1_Sept02_2020.wiff	Wiff

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Project description:<p>This study investigates lipid dysregulation in calcific aortic valve stenosis (CAVS) by analyzing lipid profiles in valve tissues from 99 patients across different disease severities (mild, moderate, severe) using liquid chromatography-mass spectrometry (LC-MS). The results reveal distinct lipid alterations that correspond to disease progression, with significant correlations between diacylglycerol (DG) and alkyl lysophosphatidylcholine (LPC(O)) levels and key markers of valve stiffness, such as peak aortic jet velocity and mean pressure gradient. Unique lipid profiles, marked by elevated cholesteryl esters and triacylglycerols, were identified in fast-progressing cases. Additionally, plasma lipids TG 52:4 and TG 54:4 emerged as promising non-invasive diagnostic markers, surpassing traditional markers in diagnostic performance. This study highlights the potential of specific lipidomic pathways as therapeutic targets in CAVS, given the current lack of effective pharmacological treatments.</p>

2025-06-25 | MTBLS6622 | MetaboLights

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Exploring molecular profiles of osteogenically differentiated aortic valvular interstitial cells

Project description:Aortic valve calcifications are often associated with calcium deposition and tissue mineralization, resulting in stiffness and dysfunction. To better understand the diversity of molecular and cellular processes for calcification in valve structures, we isolated human aortic valve interstitial cells (AVICs) and exposed them to calcification stimulation. RNA-seq revealed that in response to calcified stimuli, AVIC activates a robust ossification program, although the signaling pathways, cellular processes, and osteogenesis-related markers involved are diverse. In conclusion, this study provides a wealth of information suggesting that the pathogenesis of aortic valve calcification may be much more than previously understood.

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A novel long noncoding RNA SNHG3 promotes osteoblast differentiation through BMP2 upregulation in calcific aortic valve disease

Project description:The role of long noncoding RNAs (lncRNAs) in calcific aortic valve disease (CAVD) remains largely elusive. This study aims to report a novel therapeutic lncRNA, SNHG3, and elucidate its role in CAVD. Based on high-throughput transcriptomic sequencing of human aortic valves, SNHG3 is among the most highly expressed lncRNAs in CAVD. Furthermore, SNHG3 upregulation is verified in human calcified aortic valves, osteoblastic human aortic valve interstitial cells (hVICs), and aortic valve tissues in CAVD mice. Moreover, knockdown of SNHG3 with antisense oligonucleotide markedly ameliorates aortic valve calcification in high cholesterol diet-treated ApoE-/- mice, as evidenced by reduced calcium deposition in the aortic valve leaflets, improved echocardiographic parameters, and decreased osteogenic differentiation markers (RUNX2, osteopontin, and osteocalcin) in aortic valves. Consistent with these in vivo findings, SNHG3 overexpression aggravates the calcification of hVICs, while knockdown of SNHG3 alleviates the process of differential calcification. Transcriptomics sequencing, gene set enrichment analyses, RNA-pull down, RNA immunoprecipitation and chromatin immunoprecipitation-qPCR show that SNHG3 physically interacts with polycomb repressive complex 2 to suppress the H3K27 tri-methylation BMP2 locus, which in turn activates BMP2 expression and signaling pathways. Taken together, SNHG3 promotes aortic valve calcification by upregulating BMP2, which might be a novel therapeutic target in human CAVD.

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2024-10-17 | PXD043062 | Pride

Exploring the expression pattern of circRNA in the aortic valve

Project description:Calcific Aortic Valve Disease (CAVD) is a common heart valve condition, often characterized by severe narrowing of the aortic valve. It lacks pharmaceutical treatments and typically requires aortic valve replacement surgery, imposing a significant burden on healthcare resources.This study reports the expression profile of circRNAs in the aortic valve tissues of CAVD patients and a normal control group (non-CAVD). We collected aortic valve tissue samples from three CAVD patients who underwent aortic valve replacement surgery due to severe aortic valve stenosis, as well as aortic valve samples from non-CAVD patients who either received heart transplant surgery (recipient heart) or had their aortic valve removed due to aortic dissection. Overall, our research reveals the significant role of circRNAs in the progression of CAVD. CircRNAs, a class of circular non-coding RNA molecules, are actively studied for their functions and regulatory mechanisms within cells. These findings contribute to a deeper understanding of the molecular mechanisms underlying CAVD, particularly the potential involvement of circRNAs in this disease.

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Inhibitory Role of Notch1 in Calcific Aortic Valve Disease

Project description:Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD) are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs). We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of expression Sox9 has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism. 3 samples of aortic valve interstitial cells treated with DAPT were compared with 3 samples of aortic valve interstitial cells treated with DMSO

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Development of gene expression signatures of ascending aorta of the patients with bicuspid aortic valve compared to tricuspid aortic valve.

Project description:Bicuspid aortic valve is well known as a risk factor of dilation of ascending aorta. But the mechanisms of dialation are unknown. Morever, patients with bicuspid aortic valve tend to be aortic valve disease at younger age. After aortic valve surgery, if ascending aorta is dilated, the patient must be performed re-operation. For that reason, surgery for aortic root or ascending aorta is recommended to patient with bicuspid aortic valve with dilated ascending aorta. We thought that abnormality of cell cycle of the structure protein participated in ascending aorta dilation of patient with bicuspid aortic valve. We resected the wall of the ascending aota from patient undergoing aortic valve replacement for aortic valve stenosis during operation, and performed immunohistochemical staining for akt. Anti Akt antibodys were stained much on aortic media with bicuspoed aortic valve. Akt is a protein that is involved in mTOR / PI3K, and modulate the cell differenciation and proliferation. Further, the same samples were analyzed using a microarray method. On bicuspid aortic valve patients, the expression of TSC2 is reduced, and GβL is increased. TSC2 inhibit this pathway, and MLST8 activate this pathway. In the ascending aorta of BAV patients, PI3K / mTOR system is considered to be activated. When this pathway is activated, cell proliferation and cytodifferentiation are promoted abnormally,

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Transcription profiling of pig endothelial cells from animials fed high or low cholesterol diet shows brief hypercholesterolemia induces side-specific protective changes in pig aortic valve endothelia

Project description:The study demonstrates (i) spatial heterogeneity of endothelial responses to hypercholesterolemia in the aortic valve, (ii) that endothelial metabolism is not dysfunctional in early focal lipid insudation, and (iii) that protective endothelial pathways induced by hypercholesterolemia may initially inhibit the onset of AVS in regions most susceptible.

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