ArticleBMC cardiovascular disorders2023
CircHIPK3 relieves vascular calcification via mediating SIRT1/PGC-1α/MFN2 pathway by interacting with FUS.
Article in BMC cardiovascular disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- The dark genome in cardiovascular medicine.European heart journal · 2026Review
- Exploring the role of circ-GALK2 in vascular smooth muscle cell calcification: mechanisms and implications.European journal of medical research · 2025Article
- Functions and application of circRNAs in vascular aging and aging-related vascular diseases.Journal of nanobiotechnology · 2025Review
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Mechanism and treatment of Sirtuin family in vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- The role and mechanism of protein post‑translational modification in vascular calcification (Review).Experimental and therapeutic medicine · 2024Review
- Nitrogen-containing bisphosphonate induces enhancement of OPG expression and inhibition of RANKL expression via inhibition of farnesyl pyrophosphate synthase to inhibit the osteogenic differentiation and calcification in vascular smooth muscle cells.BMC cardiovascular disorders · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCircular RNAs (circRNAs) have been reported to regulate the biological processes of human diseases. CircHIPK3 has been implicated in vascular calcification, but the downstream regulatory mechanisms remain unclear. Our study aimed to understand the regulatory function of circHIPK3 in vascular calcification.
methodsCircHIPK3 expression in atherosclerosis (AS) serum samples and vascular smooth muscle cells (VSMCs) calcification model was assessed by quantitative real-time polymerase chain reaction (qRT-PCR). The binding relationships between fused in sarcoma (FUS) and circHIPK3 or sirtuin 1 (SIRT1) were verified by RNA immunoprecipitation (RIP) assay and RNA pull-down assays. Alkaline phosphatase (ALP) activity and alizarin red staining assays were performed to evaluate the biological effect of β-glycerophosphate (β-GP) and circHIPK3 on calcium deposition. qRT-PCR and western blot assays were used to examine the effect of β-GP, circHIPK3, SIRT1, mitofusin 2 (MFN2), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) on VSMCs calcification and the expression of calcification-related proteins.
resultsIn AS serum samples and VSMCs calcification model, the expression of circHIPK3 was significantly reduced. CircHIPK3 overexpression inhibited ALP activity and calcium deposition in β-GP-induced VSMCs. Moreover, circHIPK3 could recruit FUS to further stabilize SIRT1 mRNA. CircHIPK3 promoted MFN2 expression to alleviate VSMCs calcification via activating SIRT1/PGC-1α signaling.
conclusionThe positive regulation of circHIPK3/FUS/SIRT1/PGC-1α/MFN2 signaling pathway contributed to the alleviate VSMCs calcification, revealing a novel regulatory axis for vascular calcification.
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