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| Genes | PD | Aging |
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| MMP2 | Compared with healthy individuals (controls), metalloproteases (MMP-2, MMP-9) cascade in the initiation and progression of inflammatory bone resorption and periodontal soft tissue destruction in patients with periodontitis. [27]. | Skin aging with age or premature aging caused by light promotes cellular inflammation, ROS production, and the increase of hydrogen peroxide, and matrix metalloproteinase (MMP2) expression is upregulated. [28]. |
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| PDGFRB | PDGF receptor- (PDGFR-) β on periodontal cells is a crucial element for various functions, such as wound healing in periodontal tissue, and their expression decreases when subjected to fluid shear stress [29]. | Oxidative stress-induced senescent vascular smooth muscle cells were obviously desensitized to stimulation by platelet-derived growth factor- (PDGF-) BB, which may have been caused by suppression of promoter activity, transcription, translation, and activation levels of PDGF receptor- (PDGFR-) β [30]. |
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| CTGF | CTGF promotes the fusion of preosteoclasts by downregulating Bcl6 and subsequently increasing the expression of dendritic cell-specific transmembrane protein in periodontitis [31]. | An upregulation of CTGF expression has been demonstrated in senescent cells [32]. |
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| CD34 | The highest concentration of CD34+ cells was observed in the group of patients with advanced periodontal disease [33].
Treatment of periodontitis has neutral effects on peripheral endothelial function but significantly decreases circulating CD34(+) cell count [34]. | The absolute number of circulating CD34(+) cells progressively and significantly decreased with advancing age [35]. |
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| CXCL12 | CXCL12 (SDF-1alpha) may be involved in the immune defense pathway activated during periodontal disease. Upon the development of diseased tissues, CXCL12 (SDF-1alpha) levels increase and may recruit host defensive cells into sites of inflammation [36]. | CXCR4 pathway stimulated by CXCL12 regulated AKT activation, CREB phosphorylation, and P53 level to affect the process of aging and Alzheimer’s disease [37]. |
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| VIM | VIM expression is also regulated by TGF and proinflammatory cytokines. VIM expression increased significantly as periodontitis developed severe [38]. | It was reported that VIM expression in was significantly increased in aged skin fibroblasts [39]. |
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| ACTA2 | None | Seven aging molecular phenotype-relevant key genes (ACTA2, CALD1, LMOD1, MYH11, MYL9, MYLK, and TAGLN) were identified, which were specifically upregulated in tumors and in relation to dismal prognosis [40]. |
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| COL4A2 | COL4A2 in the ECM promotes osteogenic differentiation of PDLSCs through negative regulation of the Wnt/β-catenin pathway, which can be used as a potential therapeutic strategy to repair bone defects [41]. | Aging suppresses the expression levels of Col4a1 and Col4a2 and affects basement membrane-related factors in the steady state [42]. |
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| TAGLN | None | Seven aging molecular phenotype-relevant key genes (ACTA2, CALD1, LMOD1, MYH11, MYL9, MYLK, and TAGLN) were identified, which were specifically upregulated in tumors and in relation to dismal prognosis [40]. |
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| IL2RG | None | The expression levels of IL7, IL2RG, and IL7R were significantly lower in the 90-year-old adults, as compared with the middle-aged offspring [43]. |
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