ArticleBone research2022
LncRNA GACAT2 binds with protein PKM1/2 to regulate cell mitochondrial function and cementogenesis in an inflammatory environment.
Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The trial behind it
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Who cites it
40 citing papers in PubMed, 76 citations in OpenAlex.
- Melatonin ameliorates inflammation-induced mitochondrial dysfunction and cementoblastic differentiation in cells by regulating the METTL3/LINC01444/HSPD1 axis.Fundamental research · 2026Article
- Application of Intracellular Vesicles Surpass Extracellular Vesicles in Regenerative Repair of Inflammatory Bone Defects via the LAMA4-Mediated YAP/TAZ Signalling.Journal of extracellular vesicles · 2026Article
- Fibroblast-derived exosomes induce macrophage pyroptosis to mediate orthodontic bone remodeling through the mtDNA/NLRP3 axis.Journal of nanobiotechnology · 2026Article
- FRZB regulates the osteogenic differentiation of periodontal ligament stem cells in an inflammatory microenvironment through Wnt5a-mitochondrial axis.Cell regeneration (London, England) · 2026Article
- Targeted Inhibition of P. gingivalis OMV-derived TsRNA by tetrahedral framework nucleic acids promotes periodontal regeneration.Journal of nanobiotechnology · 2026Article
- Periodontitis and cardiovascular diseases: bridging the gap through mitochondrial dysfunction.Frontiers in oral health · 2026Review
- Periodontal ligament stem cells in tissue remodeling: from mechanical forces to inflammatory signals.Stem cell research & therapy · 2025Review
- Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025Review
- Macrophage junctional adhesion molecule-like (JAML) protein promotes NLRP3 inflammasome activation in the development of atherosclerosis.Cell death and differentiation · 2025Article
- GRK2-mediated phosphorylation and de-succinylation of PKM2 reduce macrophage glycolysis in rheumatoid arthritis.Acta pharmacologica Sinica · 2025Article
- EIF4A3-induced circPRKAR1B promotes esophageal squamous cell carcinoma progression through binding PKM2 to regulate NF-κB induced CCL3 secretion.Cancer cell international · 2025Article
- Diabetes and periodontitis: the role of a high-glucose microenvironment in periodontal tissue cells and corresponding therapeutic strategies.Stem cell research & therapy · 2025Review
- cGAMP-targeting injectable hydrogel system promotes periodontal restoration by alleviating cGAS-STING pathway activation.Bioactive materials · 2025Article
- Progress in Basic Research and Clinical Strategies for Cementum Regeneration.International dental journal · 2025Review
- The role of PKM2-mediated metabolic reprogramming in the osteogenic differentiation of BMSCs under diabetic periodontitis conditions.Stem cell research & therapy · 2025Article
- SLC30A4-AS1 Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via the Alternative Splicing of TP53BP1.Cell proliferation · 2025Article
- Mendelian randomization analysis and molecular mechanism study of childhood asthma and obstructive sleep apnea.Human genetics · 2025Article
- GMRSP encoded by lncRNA H19 regulates metabolic reprogramming and alleviates aortic dissection.Nature communications · 2025Article
- LncRNA NR_045147 modulates osteogenic differentiation and migration in PDLSCs via ITGB3BP degradation and mitochondrial dysfunction.Stem cells translational medicine · 2025Article
- Cementum regeneration strategies: Insights from development and periodontal microenvironment.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Periodontal ligament stem cells (PDLSCs) are a key cell type for restoring/regenerating lost/damaged periodontal tissues, including alveolar bone, periodontal ligament and root cementum, the latter of which is important for regaining tooth function. However, PDLSCs residing in an inflammatory environment generally exhibit compromised functions, as demonstrated by an impaired ability to differentiate into cementoblasts, which are responsible for regrowing the cementum. This study investigated the role of mitochondrial function and downstream long noncoding RNAs (lncRNAs) in regulating inflammation-induced changes in the cementogenesis of PDLSCs. We found that the inflammatory cytokine-induced impairment of the cementogenesis of PDLSCs was closely correlated with their mitochondrial function, and lncRNA microarray analysis and gain/loss-of-function studies identified GACAT2 as a regulator of the cellular events involved in inflammation-mediated mitochondrial function and cementogenesis. Subsequently, a comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and parallel reaction monitoring (PRM) assays revealed that GACAT2 could directly bind to pyruvate kinase M1/2 (PKM1/2), a protein correlated with mitochondrial function. Further functional studies demonstrated that GACAT2 overexpression increased the cellular protein expression of PKM1/2, the PKM2 tetramer and phosphorylated PKM2, which led to enhanced pyruvate kinase (PK) activity and increased translocation of PKM2 into mitochondria. We then found that GACAT2 overexpression could reverse the damage to mitochondrial function and cementoblastic differentiation of PDLSCs induced by inflammation and that this effect could be abolished by PKM1/2 knockdown. Our data indicated that by binding to PKM1/2 proteins, the lncRNA GACAT2 plays a critical role in regulating mitochondrial function and cementogenesis in an inflammatory environment.
Identifiers
What OpenQuestion holds
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.