ArticleOncology letters2018
SMOC1 silencing suppresses the angiotensin II-induced myocardial fibrosis of mouse myocardial fibroblasts via affecting the BMP2/Smad pathway.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Exosomal miR-15a-5p from cardiomyocytes promotes myocardial fibrosis.Molecular and cellular biochemistry · 2025Article
- Molecular Interplay in Cardiac Fibrosis: Exploring the Functions of RUNX2, BMP2, and Notch.Reviews in cardiovascular medicine · 2024Review
- Dynamic alterations in metabolomics and transcriptomics associated with intestinal fibrosis in a 2,4,6-trinitrobenzene sulfonic acid-induced murine model.Journal of translational medicine · 2023Article
- Plasma metabolomics and gene regulatory networks analysis reveal the role of nonstructural SARS-CoV-2 viral proteins in metabolic dysregulation in COVID-19 patients.Scientific reports · 2022Article
- Yi-Shen-Hua-Shi Granule Alleviates Adriamycin-Induced Glomerular Fibrosis by Suppressing the BMP2/Smad Signaling Pathway.Frontiers in pharmacology · 2022Article
- SMOC1 and IL-4 and IL-13 Cytokines Interfere with CaThe Journal of investigative dermatology · 2021Article
- DNA Methylation Analysis Identifies Patterns in Progressive Glioma Grades to Predict Patient Survival.International journal of molecular sciences · 2021Article
- Clinical Prescription-Protein-Small Molecule-Disease Strategy (CPSD), A New Strategy for Chinese Medicine Development: A Case Study in Cardiovascular Diseases.Frontiers in pharmacology · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
SPARC-related modular calcium binding 1 (SMOC1) represents a vital member of the SPARC matricellular protein family that regulates cell matrix interaction through binding to cell-surface receptors. The present study aimed to investigate the roles and molecular mechanisms of SMOC1 silencing on the fibrosis of myocardial fibroblasts (MFBs). Cell Counting kit-8 and flow cytometry assays were performed to determine cell viability and reactive oxygen species (ROS) content, respectively. ELISA was performed to detect the expression of associated cytokines and matrix proteins. Western blot analysis and reverse transcription-quantitative polymerase chain reaction assays were used to evaluate the expression of associated proteins and mRNAs, respectively. The results revealed that SMOC1 silencing suppressed the cell viability of angiotensin II (Ang II)-treated MFBs. SMOC1 silencing reduced the ROS content and oxidative stress in MFBs in response to Ang II. Furthermore, SMOC1 silencing downregulated the expression levels of fibrosis-associated proteins in Ang II-treated MFBs. SMOC1 silencing affected the bone morphogenetic protein 2 (BMP2)/Smad signaling pathway in Ang II-treated MFBs. In conclusion, the results of the present study suggested that SMOC1 silencing suppressed the Ang II-induced myocardial fibrosis of mouse MFBs through affecting the BMP2/Smad signaling pathway.
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