ArticlePloS one2018
SMOC2 inhibits calcification of osteoprogenitor and endothelial cells.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- Inhibition of cyclin-dependent kinase 8 modulates chondrocyte transition to hypertrophy and provides in vivo protection against spontaneous osteoarthritis.Bone research · 2026Article
- Article
- Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025Review
- Identification of signature genes and subtypes for heart failure diagnosis based on machine learning.Frontiers in cardiovascular medicine · 2025Article
- Uncovering hub genes and immunological characteristics for heart failure utilizing RRA, WGCNA and Machine learning.International journal of cardiology. Heart & vasculature · 2024Article
- Identification of Key Osteoporosis Genes Through Comparative Analysis of Men's and Women's Osteoblast Transcriptomes.Calcified tissue international · 2023Article
- SMOC2 promoted vascular smooth muscle cell proliferation, migration, and extracellular matrix degradation by activating BMP/TGF-β1 signaling pathway.Journal of clinical biochemistry and nutrition · 2023Article
- Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling.Stem cells international · 2023Article
- microRNA-148a in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2.Molecular biotechnology · 2022Article
- Single-Cell Analysis Uncovers Osteoblast Factor Growth Differentiation Factor 10 as Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation Associated with Plaque Rupture in Human Carotid Artery Disease.International journal of molecular sciences · 2022Article
- Suppression of SMOC2 alleviates myocardial fibrosisFrontiers in cardiovascular medicine · 2022Article
- LncRNA LINC01857 drives pancreatic adenocarcinoma progression via modulating miR-19a-3p/SMOC2.Clinics (Sao Paulo, Brazil) · 2022Article
- Contributions of the Endothelium to Vascular Calcification.Frontiers in cell and developmental biology · 2021Review
- Genome Wide Epistasis Study of On-Statin Cardiovascular Events with Iterative Feature Reduction and Selection.Journal of personalized medicine · 2020Article
- Deficiency of the SMOC2 matricellular protein impairs bone healing and produces age-dependent bone loss.Scientific reports · 2020Article
- Secreted modular calcium-binding proteins in pathophysiological processes and embryonic development.Chinese medical journal · 2019Review
- Transposable element-mediated structural variation analysis in dog breeds using whole-genome sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue calcification is an important physiological process required for the normal structure and function of bone. However, ectopic or excessive calcification contributes to diseases such as chondrocalcinosis, to calcium deposits in the skin or to vascular calcification. SMOC2 is a member of the BM-40/osteonectin family of calcium-binding secreted matricellular proteins. Using osteoprogenitor MC3T3-E1 cells stably overexpressing SMOC2, we show that SMOC2 inhibits osteogenic differentiation and extracellular matrix mineralization. Stable Smoc2 knockdown in these cells had no effect on mineralization suggesting that endogenous SMOC2 is not essential for the mineralization process. Mineralization in MC3T3-E1 cells overexpressing mutant SMOC2 lacking the extracellular calcium-binding domain was significantly increased compared to cells overexpressing full length SMOC2. When SMOC2 overexpressing cells were cultured in the presence of extracellular calcium supplementation, SMOC2's inhibitory effect on calcification was rescued. Our observations were translationally validated in primary human periosteal-derived cells. Furthermore, SMOC2 was able to impair mineralization in transdifferentiated human umbilical vein endothelial cells. Taken together, our data indicate that SMOC2 can act as an inhibitor of mineralization. We propose a possible role for SMOC2 to prevent calcification disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.