ArticleInternational journal of molecular sciences2025
Activating Transcription Factor 3 (ATF3) Regulates Cellular Senescence and Osteoclastogenesis via STAT3/ERK and p65/AP-1 Pathways in Human Periodontal Ligament Cells.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Intracellular Calcium Overload Promotes NFATc1-ATF3 Activation and Induces the Senescence-Associated Phenotype in Irradiated Osteocytes.Life (Basel, Switzerland) · 2026Article
- Identification of ATF3 as a Potential Key Biomarker for Hypertensive Nephropathy via Single-Cell Transcriptome Sequencing.Inflammation · 2026Article
- Circadian rhythm disruption affects cellular senescence through the BMAL1/CRY2/PER1 signaling pathway in periodontitis.Journal of molecular histology · 2026Article
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
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Authors and funding
2 authors.
Funding
Abstract
Oral cellular aging plays a critical role in the pathogenesis of chronic periodontitis and alveolar bone resorption. Although activating transcription factor 3 (ATF3) has been implicated as a senescence-associated factor, its specific role in periodontal ligament cell (PDLC) senescence remains unclear. Human PDLCs were exposed to lipopolysaccharide (LPS, 1 μg/mL) and nicotine (5 mM) for 3 days to induce senescence. ATF3 expression was silenced using siRNA. The expression of senescence-associated secretory phenotype (SASP) factors (IFNγ, IL6, IL8, TNFα, and IL1β) and the secretion of nitric oxide (NO) and prostaglandin E
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