ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Senescent Fibroblasts Drive FAP/OLN Imbalance Through mTOR Signaling to Exacerbate Inflammation and Bone Resorption in Periodontitis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- M2-Exo-derived miR-1227-5p protects against periodontitis through inhibiting USP2-dependent deubiquitination of Drp1.Journal of bioenergetics and biomembranes · 2026Article
- Bone aging: a paradigm of multiscale degeneration and targeted rejuvenation.Bone research · 2026Review
- FAM30A Induces Inflammation and Oxidative Damage in PDLSCs by Targeting miR-424-5p.International dental journal · 2026Article
- Suppression of Ciliogenesis Alleviates Cellular Senescence via AKT Signaling in Gingival Aging.Aging cell · 2026Article
- Ageing of the Oral Mucosa: Mechanisms and Consequences.International dental journal · 2026Review
- Myeloid-Derived Grancalcin Promotes Periodontal Inflammation and Pathological Bone Remodeling in Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Circadian rhythm disruption affects cellular senescence through the BMAL1/CRY2/PER1 signaling pathway in periodontitis.Journal of molecular histology · 2026Article
- Plasma exosomal fibroblast activation protein: a novel biomarker links fatty acid metabolic dysregulation to systemic lupus erythematosus.Arthritis research & therapy · 2026Article
- Proteomic profiling and pathway analyses reveal molecular signatures and immune networks in pediatric sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.Journal of nanobiotechnology · 2026Article
- Identification and characterization of fibroblast-related biomarkers and pro-inflammatory subpopulations in periodontitis by integrated transcriptomic and single-cell analysis.Scientific reports · 2026Article
- Myeloma-derived exosomal circ_0002724 promotes osteoclastogenesis through a miR-4753-3p/IFIT1 and RANK axis in myeloma bone disease.Frontiers in oncology · 2026Article
- Regulation of Mitochondrial Homeostasis: Applications of Nanobiomaterials in Age-Related Bone Diseases.International journal of nanomedicine · 2026Review
- Ultra-small coordination dihydromyricetin nanodots attenuate alveolar bone resorption in periodontitis through inhibition of ITGB3-Driven osteoclast differentiation.Materials today. Bio · 2025Article
- Emerging Roles of Extracellular Vesicles in the Pathogenesis, Diagnosis, and Therapy of Periodontitis.Biomedicines · 2025Review
- CD81eLife · 2025Article
- Senescent Fibroblasts Drive FAP/OLN Imbalance Through mTOR Signaling to Exacerbate Inflammation and Bone Resorption in Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nanozymes Empower Periodontitis Treatment: New Strategies and Clinical Application Prospects.Biomaterials research · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Fibroblast activation protein (FAP), predominantly expressed in activated fibroblasts, plays a key role in inflammatory bone diseases, but its role in periodontitis remains unclear. Accordingly, this study identified a positive association between FAP levels and periodontitis susceptibility using Mendelian randomization analysis. Human and mouse periodontitis tissues show elevated FAP and reduced osteolectin (OLN), an endogenous FAP inhibitor, indicating a FAP/OLN imbalance. Single-cell RNA sequencing revealed gingival fibroblasts (GFs) as the primary FAP and OLN source, with periodontitis-associated GFs showing increased reactive oxygen species, cellular senescence, and mTOR pathway activation. Rapamycin treatment restored the FAP/OLN balance in GFs. Recombinant FAP increased pro-inflammatory cytokine secretion and osteoclast differentiation in macrophages, exacerbating periodontal damage, whereas FAP inhibition reduced macrophage inflammation, collagen degradation, and bone resorption in experimental periodontitis. Therefore, senescent fibroblasts drive the FAP/OLN imbalance through mTOR activation, contributing to periodontitis progression. Consequently, targeting FAP may offer a promising therapeutic strategy for periodontitis.
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