ArticleBioactive materials2026
Metformin alleviates aging-associated periodontitis via NRF2-mediated restoration of the IRE1α dependent unfolded protein response.
Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Proteostasis disruption due to impaired unfolded protein response (UPR) is a hallmark of aging and contributes largely to cellular dysfunction, but its role and associated mechanisms in aging-associated periodontitis remain unclear. This study reveals that senescent periodontal ligament stem cells (PDLSCs) exhibit impaired NRF2/IRE1α-dependent UPR signaling, leading to increased senescence-associated secretory phenotype (SASP) and reduced osteogenesis. NRF2 overexpression restored IRE1α-dependent UPR signaling and suppressed SASP in senescent PDLSCs, whereas NRF2 knockout/inhibition showed opposite results. Mechanistically, the CUT-RUN assay indicates that NRF2 transcriptionally upregulates IRE1α, thereby restoring UPR activity. Notably, we found that metformin, a known anti-aging agent, attenuated SASP by enhancing NRF2/IRE1α-dependent UPR signaling in PDLSCs. To enhance the therapeutic efficacy of metformin, we developed a senescence-targeted, metformin-releasing nanocomposite hydrogel (TAM-GM@Met) by coating metformin-loaded mesoporous polydopamine nanoparticles with galactose (GM) and encapsulating them within a tannic acid and Ag-MOF-based hydrogel (TAM). This delivery system effectively upregulated NRF2/IRE1α-dependent UPR signaling, suppressed SASP
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