ArticleCell proliferation2022
LncRNA-AK137033 inhibits the osteogenic potential of adipose-derived stem cells in diabetic osteoporosis by regulating Wnt signaling pathway via DNA methylation.
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- A novel regulator in cancer initiation and progression: long noncoding RNA SHNG9.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Pooled it
- Uncovering the mechanisms of Jingui Shenqi pill alleviates type 2 diabetic osteoporosis using a combined network pharmacology and metabolomics approach.Scientific reports · 2026Article
- New Aspects of the Pathophysiology of Diabetic Bone Fragility - Type 2 Diabetes Mellitus as a Disease of Accelerated Aging.Current osteoporosis reports · 2025Review
- Accelerating Bone Healing With METTL3 Overexpressed Adipose-Derived Stem Cells in Osteoporotic Rats.Cell proliferation · 2025Article
- Linc00963 up-regulation alleviates postmenopausal osteoporosis through suppression of miR-506-3p.Journal of orthopaedic surgery and research · 2025Article
- Ovarian Endometriosis Accelerates Premature Ovarian Failure and Contributes to Osteoporosis and Cognitive Decline in Aging Mice.International journal of molecular sciences · 2025Article
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
- Inhibition of histone methyltransferase G9a promotes the osteogenic potential of bone-derived stem cells in diabetic-osteoporosis by regulating the LINC00657/miR-204-5p/IGFBP5 pathway.Frontiers in endocrinology · 2025Article
- A DNA tetrahedron-based ferroptosis-suppressing nanoparticle: superior delivery of curcumin and alleviation of diabetic osteoporosis.Bone research · 2024Article
- Curcumin can improve spinal cord injury by inhibiting DNA methylation.Molecular and cellular biochemistry · 2024Article
- Wnt10b regulates osteogenesis of adipose-derived stem cells through Wnt/β-catenin signalling pathway in osteoporosis.Cell proliferation · 2024Article
- Reactive Oxygen Species Scavenging Hydrogel Regulates Stem Cell Behavior and Promotes Bone Healing in Osteoporosis.Tissue engineering and regenerative medicine · 2023Article
- The Mission of Long Non-Coding RNAs in Human Adult Renal Stem/Progenitor Cells and Renal Diseases.Cells · 2023Review
- Epigenetic control of mesenchymal stem cells orchestrates bone regeneration.Frontiers in endocrinology · 2023Review
- Mesenchymal Stem Cell-Derived from Dental Tissues-Related lncRNAs: A New Regulator in Osteogenic Differentiation.Journal of tissue engineering and regenerative medicine · 2023Review
- Mendelian randomization to evaluate the causal relationship between liver enzymes and the risk of six specific bone and joint-related diseases.Frontiers in immunology · 2023Article
- Downregulation of DNA methyltransferase-3a ameliorates the osteogenic differentiation ability of adipose-derived stem cells in diabetic osteoporosis via Wnt/β-catenin signaling pathway.Stem cell research & therapy · 2022Article
- Biological aspects in controlling angiogenesis: current progress.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- LncRNA-AK137033 inhibits the osteogenic potential of adipose-derived stem cells in diabetic osteoporosis by regulating Wnt signaling pathway via DNA methylation.Cell proliferation · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesBone tissue engineering based on adipose-derived stem cells (ASCs) is expected to become a new treatment for diabetic osteoporosis (DOP) patients with bone defects. However, compared with control ASCs (CON-ASCs), osteogenic potential of DOP-ASCs is decreased, which increased the difficulty of bone reconstruction in DOP patients. Moreover, the cause of the poor osteogenesis of ASCs in a hyperglycemic microenvironment has not been elucidated. Therefore, this study explored the molecular mechanism of the decline in the osteogenic potential of DOP-ASCs from the perspective of epigenetics to provide a possible therapeutic target for bone repair in DOP patients with bone defects. MATERIALS AND
methodsAn animal model of DOP was established in mice. CON-ASCs and DOP-ASCs were isolated from CON and DOP mice, respectively. AK137033 small interfering RNA (SiRNA) and an AK137033 overexpression plasmid were used to regulate the expression of AK137033 in CON-ASCs and DOP-ASCs in vitro. Lentiviruses that carried shRNA-AK137033 or AK137033 cDNA were used to knockdown or overexpress AK137033, respectively, in CON-ASCs and DOP-ASCs in vivo. Hematoxylin and eosin (H&E), Masson's, alizarin red, and alkaline phosphatase (ALP) staining, micro-computed tomography (Micro-CT), flow cytometry, qPCR, western blotting, immunofluorescence, and bisulfite-specific PCR (BSP) were used to analyze the functional changes of ASCs.
resultsThe DOP mouse model was established successfully. Compared with CON-ASCs, AK137033 expression, the DNA methylation level of the sFrp2 promoter region, Wnt signaling pathway markers, and the osteogenic differentiation potential were decreased in DOP-ASCs. In vitro experiments showed that AK137033 silencing inhibited the Wnt signaling pathway and osteogenic ability of CON-ASCs by reducing the DNA methylation level in the sFrp2 promoter region. Additionally, overexpression of AK137033 in DOP-ASCs rescued these changes caused by DOP. Moreover, the same results were obtained in vivo.
conclusionsLncRNA-AK137033 inhibits the osteogenic potential of DOP-ASCs by regulating the Wnt signaling pathway via modulating the DNA methylation level in the sFrp2 promoter region. This study provides an important reference to find new targets for the treatment of bone defects in DOP patients.
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