ArticleExperimental & molecular medicine2024
Noncoding RNA regulates the expression of Krm1 and Dkk2 to synergistically affect aortic valve lesions.
Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Review
- Whole-transcriptome analysis of Aortic Stenosis reveals dysregulated RNA networks, immune cell infiltration, and NADK2 as a candidate regulator.Hereditas · 2026Article
- Dickkopf 2 serves as a novel therapeutic target and prognostic biomarker in acute myeloid leukemia targeted by evodiamine.Frontiers in medicine · 2026Article
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- Inhibition of lnc-COL6A1-6-Alleviated Osteogenic Differentiation of Valvular Interstitial Cells During Aortic Valve Calcification.Cardiovascular therapeutics · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Calcific aortic valve disease (CAVD) is becoming an increasingly important global medical problem, but effective pharmacological treatments are lacking. Noncoding RNAs play a pivotal role in the progression of cardiovascular diseases, but their relationship with CAVD remains unclear. Sequencing data revealed differential expression of many noncoding RNAs in normal and calcified aortic valves, with significant differences in circHIPK3 and miR-182-5p expression. Overexpression of circHIPK3 ameliorated aortic valve lesions in a CAVD mouse model. In vitro experiments demonstrated that circHIPK3 inhibits the osteogenic response of aortic valve interstitial cells. Mechanistically, DEAD-box helicase 5 (DDX5) recruits methyltransferase 3 (METTL3) to promote the N6-methyladenosine (m6A) modification of circHIPK3. Furthermore, m6A-modified circHIPK3 increases the stability of Kremen1 (Krm1) mRNA, and Krm1 is a negative regulator of the Wnt/β-catenin pathway. Additionally, miR-182-5p suppresses the expression of Dickkopf2 (Dkk2), the ligand of Krm1, and attenuates the Krm1-mediated inhibition of Wnt signaling. Activation of the Wnt signaling pathway significantly contributes to the promotion of aortic valve calcification. Our study describes the role of the Krm1-Dkk2 axis in inhibiting Wnt signaling in aortic valves and suggests that noncoding RNAs are upstream regulators of this process.
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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.