ArticleMolecular therapy. Nucleic acids2020
circRNA CDR1as Promotes Pulmonary Artery Smooth Muscle Cell Calcification by Upregulating CAMK2D and CNN3 via Sponging miR-7-5p.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Circular RNAs in pulmonary hypertension: Emerging biological concepts and potential mechanism.Animal models and experimental medicine · 2022Pooled it
- Review
- Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate.Cellular and molecular life sciences : CMLS · 2026Article
- Mechanisms of vascular calcification: cellular phenotype switching drives matrix remodeling and mineralized microenvironment formation.Frontiers in cardiovascular medicine · 2026Review
- Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025Review
- Circular RNAs in Cardiovascular Physiopathology: From Molecular Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Functions and application of circRNAs in vascular aging and aging-related vascular diseases.Journal of nanobiotechnology · 2025Review
- Inter-chromosomal insertions at Xq27.1 associated with retinal dystrophy induce dysregulation of LINC00632 and CDR1as/ciRS-7.American journal of human genetics · 2025Article
- Genome-wide characterization of circular RNAs in three rat models of pulmonary hypertension reveals distinct pathological patterns.BMC genomics · 2025Article
- Endothelial cells derived extracellular vesicles promote diabetic arterial calcification via circ_0008362/miR-1251-5p/Runx2 axial.Cardiovascular diabetology · 2024Article
- Levosimendan mediates the BMP/Smad axis through upregulation of circUSP34-targeted miR-1298 to alleviate pulmonary hypertension.Respiratory research · 2024Article
- RNA m6A methylation and regulatory proteins in pulmonary arterial hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- CircALMS1 Alleviates Pulmonary Microvascular Endothelial Cell Dysfunction in Pulmonary Hypertension.Journal of the American Heart Association · 2024Article
- Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities.Biomolecules · 2024Review
- Review
- ADAR1 regulates vascular remodeling in hypoxic pulmonary hypertension throughActa pharmaceutica Sinica. B · 2023Article
- CircHIPK3 relieves vascular calcification via mediating SIRT1/PGC-1α/MFN2 pathway by interacting with FUS.BMC cardiovascular disorders · 2023Article
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- Dynamic observation of circRNA and mRNA profiles in a rat model of deep vein thrombosis.Experimental and therapeutic medicine · 2023Article
- Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?Journal of clinical medicine · 2023Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has suggested that circular RNAs (circRNAs) are involved in multiple physiological processes and participate in a variety of human diseases. However, the underlying biological function of circRNAs in pulmonary hypertension (PH) is still ambiguous. Herein, we investigated the implication and regulatory effect of a typical circRNA, CDR1as, in the pathological process of vascular calcification in PH. Human pulmonary artery smooth muscle cell (HPASMC) calcification was analyzed by western blotting, immunofluorescence, alizarin red S staining, alkaline phosphatase activity analysis, and calcium deposition quantification. CDR1as targets were identified by bioinformatics analysis and validated by dual-luciferase reporter and RNA antisense purification assays. We identified that CDR1as was upregulated in hypoxic conditions and promoted a phenotypic switch of HPASMCs from a contractile to an osteogenic phenotype. Moreover, microRNA (miR)-7-5p was shown to be a target of CDR1as, and calcium/calmodulin-dependent kinase II-delta (CAMK2D) and calponin 3 (CNN3) were suggested to be the putative target genes and regulated by CDR1as/miR-7-5p. The results showed that the CDR1as/miR-7-5p/CNN3 and CAMK2D regulatory axis mediates HPASMC osteoblastic differentiation and calcification induced by hypoxia. This evidence reveals an approach to the treatment of PH.
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