ArticleStem cells (Dayton, Ohio)2024
Integrin-linked kinase control dental pulp stem cell senescence via the mTOR signaling pathway.
Article in Stem cells (Dayton, Ohio), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Stem cell senescence as a regenerative bottleneck in age-related skeletal degeneration: Mechanistic crosstalk and translational strategies.Regenerative therapy · 2026Review
- Integrin-Linked Kinase Plays an Active Role in the Regulation of Endothelial Senescence.Cells · 2026Article
- Targeting Dental Pulp Stem Cell Senescence: A Potential Strategy for Improving Regenerative Endodontic Procedures.Bioengineering (Basel, Switzerland) · 2026Article
- Resveratrol delays senescence of human dental pulp stem cells via activating the SIRT1-mitochondrial autophagy.Scientific reports · 2025Article
- Decoding Dental Stem Cell Aging: Mechanisms, Therapeutic Strategies, and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Senescence of dental pulp stem cells: phenotypes, underlying mechanisms and regulatory molecules.Human cell · 2025Review
- The prognostic and neuroendocrine implications of SLC25A29-mediated biomass signature in prostate cancer.GeroScience · 2025Article
- NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming.International journal of oral science · 2025Article
- Effects of simulated microgravity on dental pulp stem cell stemness.Journal of molecular histology · 2025Article
- Matrix vesicle-inspired delivery system based on nanofibrous chitosan microspheres for enhanced bone regeneration.Materials today. Bio · 2025Article
- Therapeutic potential of curcumin in regenerative dentistry.Frontiers in dental medicine · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Human dental pulp stem cells (HDPSCs) showed an age-dependent decline in proliferation and differentiation capacity. Decline in proliferation and differentiation capacity affects the dental stromal tissue homeostasis and impairs the regenerative capability of HDPSCs. However, which age-correlated proteins regulate the senescence of HDPSCs remain unknown. Our study investigated the proteomic characteristics of HDPSCs isolated from subjects of different ages and explored the molecular mechanism of age-related changes in HDPSCs. Our study showed that the proliferation and osteogenic differentiation of HDPSCs were decreased, while the expression of aging-related genes (p21, p53) and proportion of senescence-associated β-galactosidase (SA-β-gal)-positive cells were increased with aging. The bioinformatic analysis identified that significant proteins positively correlated with age were enriched in response to the mammalian target of rapamycin (mTOR) signaling pathway (ILK, MAPK3, mTOR, STAT1, and STAT3). We demonstrated that OSU-T315, an inhibitor of integrin-linked kinase (ILK), rejuvenated aged HDPSCs, similar to rapamycin (an inhibitor of mTOR). Treatment with OSU-T315 decreased the expression of aging-related genes (p21, p53) and proportion of SA-β-gal-positive cells in HDPSCs isolated from old (O-HDPSCs). Additionally, OSU-T315 promoted the osteoblastic differentiation capacity of O-HDPSCs in vitro and bone regeneration of O-HDPSCs in rat calvarial bone defects model. Our study indicated that the proliferation and osteoblastic differentiation of HDPSCs were impaired with aging. Notably, the ILK/AKT/mTOR/STAT1 signaling pathway may be a major factor in the regulation of HDPSC senescence, which help to provide interventions for HDPSC senescence.
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