ArticleCardiovascular research2022
SPARC-related modular calcium binding 1 regulates aortic valve calcification by disrupting BMPR-II/p-p38 signalling.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Identification of Potential Proteins Interacting with α-Galactosidase A to Analyze the Pathogenesis of Fabry Disease.International journal of molecular sciences · 2026Article
- The Role and Mechanism of Gut Microbiota and Metabolites in Vascular Calcification.International journal of molecular sciences · 2026Review
- Screening of serum biomarkers for coronary artery calcification using DIA quantitative proteomics and construction of a regression model.Frontiers in cardiovascular medicine · 2026Article
- VAPB Promotes Osteogenic Differentiation in Aortic Valve Interstitial Cells via Activation of the SMAD Signaling Pathway.Current medicinal chemistry · 2026Article
- SMOC2 promotes peritoneal metastasis of gastric cancer involving Wnt/β-catenin pathway modulation and inducing angiogenesis.Clinical and experimental medicine · 2025Article
- Genetic Insights into Peripheral Artery Disease: A Narrative Review.Biomedicines · 2025Review
- Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene.Nature communications · 2025Article
- Knockdown of PARM1 Alleviates Aortic Valve Calcification via the PRKCH-MAPK Signaling Pathway.JACC. Basic to translational science · 2025Article
- Severe cardiac valvular calcification in two Chinese brothers with mandibuloacral dysplasia type A: a case report.Frontiers in cardiovascular medicine · 2025Article
- A novel mouse model of calcific aortic valve stenosis.Animal models and experimental medicine · 2024Article
- A new perspective on intervertebral disc calcification-from bench to bedside.Bone research · 2024Review
- A Novel LncRNA SNHG3 Promotes Osteoblast Differentiation Through BMP2 Upregulation in Aortic Valve Calcification.JACC. Basic to translational science · 2022Article
- The management of bone defect using long non-coding RNA as a potential biomarker for regulating the osteogenic differentiation process.Molecular biology reports · 2022Review
- Marine-Derived Piericidin Diglycoside S18 Alleviates Inflammatory Responses in the Aortic Valve via Interaction with Interleukin 37.Oxidative medicine and cellular longevity · 2022Article
- Hepatokines and Non-Alcoholic Fatty Liver Disease: Linking Liver Pathophysiology to Metabolism.Biomedicines · 2021Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAortic valve calcification is more prevalent in chronic kidney disease accompanied by hypercalcemia. Secreted protein acidic and rich in cysteine (SPARC)-related modular calcium binding 1 (SMOC1) is a regulator of BMP2 signalling, but the role of SMOC1 in aortic valve calcification under different conditions has not been studied. This study aimed to investigate the roles of SMOC1 in aortic valve calcification under normal and high calcium conditions, focusing on the effects on aortic valve interstitial cells (AVICs). METHODS AND
resultsSMOC1 was expressed by aortic valve endothelial cells and secreted into the extracellular matrix in non-calcific valves and downregulated in calcific aortic valves. In vitro studies demonstrated that HUVEC secreted SMOC1 could enter the cytoplasm of AVICs. Overexpression of SMOC1 attenuated warfarin-induced AVIC calcification but promoted high calcium/phosphate or vitamin D-induced AVIC and aortic valve calcification by regulating BMP2 signalling both in vitro and in vivo. Co-immunoprecipitation revealed that SMOC1 binds to BMP receptor II (BMPR-II) and inhibits BMP2-induced phosphorylation of p38 (p-p38) via amino acids 372-383 of its EF-hand calcium-binding domain. Inhibition of p-p38 by the p38 inhibitor SB203580 blocked the effects of SMOC1 on BMP2 signalling and AVIC calcification induced by high calcium/phosphate medium. In high-calcium-treated AVICs, SMOC1 lost its ability to bind to BMPR-II, but not to caveolin-1, promoting p-p38 and cell apoptosis due to increased expression of BMPR-II and enhanced endocytosis.
conclusionsThese observations support that SMOC1 works as a dual-directional modulator of AVIC calcification by regulating p38-dependent BMP2 signalling transduction according to different extracellular calcium concentrations.
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