ArticleCell death and differentiation2022
LncRNA NEAT1 controls the lineage fates of BMSCs during skeletal aging by impairing mitochondrial function and pluripotency maintenance.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.
- Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment.Biomolecules · 2025Pooled it
- LncRNA Gm44981 modulates EZH2-H3K27me3-p21 axis to suppress mesangial cell senescence and kidney aging.Renal failure · 2026Article
- Review
- Paraspeckle-Mediated Integration of Nuclear RNA Regulation in Skeletal Homeostasis and Pathological Disorder.Calcified tissue international · 2026Review
- GLP-1 regulates osteo-adipogenic fate of BMSCs via HIF-2-AKT signaling and supports trabecular bone in glucocorticoid-induced osteoporosis.Stem cell reports · 2026Article
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Targeting the Gpr125-Gper1 axis: a novel osteogenic signaling pathway with therapeutic potential against osteoporosis.Journal of translational medicine · 2026Article
- Melatonin ameliorates inflammation-induced mitochondrial dysfunction and cementoblastic differentiation in cells by regulating the METTL3/LINC01444/HSPD1 axis.Fundamental research · 2026Article
- Diagnostic value of LncRNA JPX in osteoporotic fracture (OPF) and its role in inhibiting osteogenic differentiation by targeting miR-219a-5p.Hereditas · 2026Article
- Retinoic Acid and Long Noncoding RNAs Crosstalk: Implications for Neuronal Differentiation and Diseases.Molecular neurobiology · 2026Review
- Immune-evasive stem cells: engineering tolerance and reprogramming microenvironments for regenerative therapy.Stem cell research & therapy · 2026Review
- Application Strategies of Bone Marrow Mesenchymal Stromal Cells in Bone-Related Diseases.Cell proliferation · 2026Review
- Single-Cell Triomics Analysis of Tumor Cells Infiltrating Patient-Derived Breast Cancer Scaffolds.The American journal of pathology · 2026Article
- Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2-Mediated Cytoskeletal-Nuclear Mechanotransduction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The DNA Methylation-Autophagy Axis: A Driver of MSC Fate Imbalance in Skeletal Aging and Osteoporosis.Biology · 2026Review
- Blockade of calcium-activated chloride channel ANO1 ameliorates ionizing radiation-induced intestinal injury.Journal of advanced research · 2026Article
- Long non-coding RNAs and accelerated aging in bipolar disorder.Neuroscience applied · 2026Review
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- A triterpene-enriched natural extract fromPharmaceutical biology · 2025Article
- Hyperoside, a flavonoid, inducesScience advances · 2025Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Aged bone marrow mesenchymal stem cells (BMSCs) exhibit aberrant self-renewal and lineage specification, which contribute to imbalanced bone-fat and progressive bone loss. In addition to known master regulators of lineage commitment, it is crucial to identify pivotal switches governing the specific differentiation fate of aged BMSCs. Here, we profiled differences in epigenetic regulation between adipogenesis and osteogenesis and identified super-enhancer associated lncRNA nuclear-enriched abundant transcript 1 (NEAT1) as a key bone-fat switch in aged BMSCs. We validated that NEAT1 with high enhancer activity was transcriptionally activated by ATF2 and directed aged BMSCs to a greater propensity to differentiate toward adipocytes than osteoblasts by mediating mitochondrial function. Furthermore, we confirmed NEAT1 as a protein-binding scaffold in which phosphorylation modification of SOX2 Ser249/250 by CDK2 impaired SOX2/OCT4 complex stability and dysregulated downstream transcription networks of pluripotency maintenance. In addition, by sponging miR-27b-3p, NEAT1 upregulated BNIP3L, BMP2K, and PPARG expression to shape mitochondrial function and osteogenic/adipogenic differentiation commitment, respectively. In extracellular communication, NEAT1 promoted CSF1 secretion from aged BMSCs and then strengthened osteoclastic differentiation by extracellular vesicle delivery. Notably, Neat1 small interfering RNA delivery induced increased bone mass in aged mice and decreased fat accumulation in the bone marrow. These findings suggest that NEAT1 regulates the lineage fates of BMSCs by orchestrating mitochondrial function and pluripotency maintenance, and might be a potential therapeutic target for skeletal aging.
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