Involvement of the visfatin/toll-like receptor 4 signaling axis in human dental pulp cell senescence: Protection via toll-like receptor 4 blockade

Ok, Chang Youp; Park, Sera; Jang, Hye-Ock; Bae, Moon‐Kyoung; Bae, Soo-Kyung

doi:10.1016/j.jds.2022.10.008

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Cited by 5 publications

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“…A study has reported that toll-like receptor 4 (TLR4) is involved in regulating cellular senescence in hDPSCs. 33 TLR4 is a molecular initiator of cellular senescence, and visfatin induces cellular senescence via TLR4 in hDPSCs. Moreover, serine metabolism and one carbon unit contribute to hDPSCs aging by providing less methyl donor to DNA methylation.…”

Section: Discussionmentioning

confidence: 99%

Lysine demethylase 3A promotes chondrogenic differentiation of aged human dental pulp stem cells

Sun

Bai

Chen

et al. 2024

Journal of Dental Sciences

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Section: Discussionmentioning

confidence: 99%

Lysine demethylase 3A promotes chondrogenic differentiation of aged human dental pulp stem cells

Sun

Bai

Chen

et al. 2024

Journal of Dental Sciences

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Inducing cyclooxygenase-2 expression, prostaglandin E2 and prostaglandin F2α production of human dental pulp cells by activation of toll-like receptor-3, mitogen-activated protein kinase kinase/extracellular signal-regulated kinase and p38 signaling

Chang,

Wu,

Chen

et al. 2024

Journal of Dental Sciences

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Toll-like receptor 4 (TLR4): new insight immune and aging

Kim,

Lee

et al. 2023

Immun Ageing

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TLR4, a transmembrane receptor, plays a central role in the innate immune response. TLR4 not only engages with exogenous ligands at the cellular membrane’s surface but also interacts with intracellular ligands, initiating intricate intracellular signaling cascades. Through MyD88, an adaptor protein, TLR4 activates transcription factors NF-κB and AP-1, thereby facilitating the upregulation of pro-inflammatory cytokines. Another adapter protein linked to TLR4, known as TRIF, autonomously propagates signaling pathways, resulting in heightened interferon expression. Recently, TLR4 has garnered attention as a significant factor in the regulation of symptoms in aging-related disorders. The persistent inflammatory response triggered by TLR4 contributes to the onset and exacerbation of these disorders. In addition, alterations in TLR4 expression levels play a pivotal role in modifying the manifestations of age-related diseases. In this review, we aim to consolidate the impact of TLR4 on cellular senescence and aging-related ailments, highlighting the potential of TLR4 as a novel therapeutic target that extends beyond immune responses.

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Involvement of the visfatin/toll-like receptor 4 signaling axis in human dental pulp cell senescence: Protection via toll-like receptor 4 blockade

Cited by 5 publications

References 38 publications

Lysine demethylase 3A promotes chondrogenic differentiation of aged human dental pulp stem cells

Lysine demethylase 3A promotes chondrogenic differentiation of aged human dental pulp stem cells

Inducing cyclooxygenase-2 expression, prostaglandin E2 and prostaglandin F2α production of human dental pulp cells by activation of toll-like receptor-3, mitogen-activated protein kinase kinase/extracellular signal-regulated kinase and p38 signaling

Toll-like receptor 4 (TLR4): new insight immune and aging

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