ArticleMolecular and cellular biochemistry2021
Overexpression of HOTAIR attenuates Pi-induced vascular calcification by inhibiting Wnt/β-catenin through regulating miR-126/Klotho/SIRT1 axis.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Review
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Association between serum alpha Klotho levels and the likelihood of abdominal aortic calcification.Scientific reports · 2026Article
- Mechanism and treatment of Sirtuin family in vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- lncRNA HOTAIR and Cardiovascular diseases.Functional & integrative genomics · 2024Review
- Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation.Theranostics · 2024Article
- LncRNA HOX transcript antisense RNA mediates hyperglycemic-induced injury in the renal tubular epithelial cell via the miR-126-5pAkt axis.Aging medicine (Milton (N.S.W)) · 2023Article
- Review
- LncRNA HOTAIR regulates the PI3K/AKT pathway via the miR-126-3p/PIK3R2 axis to participate in synovial angiogenesis in rheumatoid arthritis.Immunity, inflammation and disease · 2023Article
- Circulating Levels of HOTAIR- lncRNA Are Associated with Disease Progression and Clinical Parameters in Type 2 Diabetes Patients.Reports of biochemistry & molecular biology · 2023Article
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- Review
- Innovative therapeutic strategies for cardiovascular disease.EXCLI journal · 2023Review
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders.Frontiers in pharmacology · 2023Review
- Nrf2-Mediated Dichotomy in the Vascular System: Mechanistic and Therapeutic Perspective.Cells · 2022Review
- Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.Life (Basel, Switzerland) · 2022Review
- Lactic acid induces fibroblast growth factor 23 (FGF23) production in UMR106 osteoblast-like cells.Molecular and cellular biochemistry · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification is one of the most common effects of macrovascular complications in patients in aging with chronic kidney disease and diabetes. Previous studies showed that HOTAIR attenuated vascular calcification via the Wnt/β-catenin-signaling pathway, yet the molecular mechanism has not been fully elucidated. This study aimed to identify the explicit molecular mechanism underlying HOTAIR regulated vascular calcification. In the phosphate (Pi)-induced calcification model of human aortic smooth muscle cells (HASMCs), we investigated whether HOTAIR was involved in the regulation of miR-126. The luciferase reporter was used to examine the effect of HOTAIR on miR-126 and miR-126 on Klotho 3'-UTR. Furthermore, we overexpressed Klotho to verify the regulation of Klotho on SIRT1, as well as their roles in mediating Pi-induced calcification in HASMCs via the Wnt/β-catenin signaling pathway. Finally, the results were verified in an in vivo mice calcification model. Overexpression of HOTAIR reduced the expression of miR-126 in Pi-induced HASMCs. Additionally, knockdown of miR-126 increased SIRT1 expression by regulating Klotho expression. An increased level of Klotho inhibited Wnt/β-catenin signaling pathway, which eventually attenuated Pi-induced HASMCs calcification. Luciferase reporter assay revealed that HOTAIR targeted miR-126 and miR-126 could directly target Klotho. Eventually, HOTAIR overexpression reversed Pi-induced calcium calcification in vivo mouse models. This study demonstrated that HOTAIR overexpression attenuated Pi-induced calcification by regulating the miR-126/Klotho/SIRT1 axis, thereby inhibiting the Wnt/β-catenin signaling pathway. It provides new potential target genes for the clinical treatment of vascular calcification.
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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.