Gigantol protects retinal pigment epithelial cells against high glucose-induced apoptosis, oxidative stress and inflammation by inhibiting MTDH-mediated NF-kB signaling pathway

Chen, You; Zhao, Tong; Han, Mengyu; Chen, Yi

doi:10.1080/08923973.2023.2247545

Cited by 1 publication

(1 citation statement)

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“…It is well-documented that NF-κB comprises both classical and alternative pathways, mediating a critical role in IVDD progression [ 22 ]. HG, known for its potency in enhancing proinflammatory cytokine production, triggers activation of both NF-κB pathways [ 29 ]. Indeed, NF-κB pharmacological inhibitors and genetic siRNA were shown to diminish HG-induced fibrotic proteins expression.…”

Section: Discussionmentioning

confidence: 99%

High glucose enhances fibrosis in human annulus fibrosus cells by activating mTOR, PKCδ, and NF-κB signaling pathways

Tseng,

Liu,

et al. 2024

Aging

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Low back pain stands as a significant factor in disability, largely resulting from intervertebral disc degeneration (IVDD). High glucose (HG) levels have been implicated in the pathogenesis of IVDD. However, the detailed mechanism of HG in IVDD is largely unknown. Our clinical results revealed that fibrosis markers such as CTGF, Col1a1, ATF4, and EIF2 are highly expressed in advanced-stage IVDD patients. Stimulation of human annulus fibrosus cells (HAFCs) with HG, but not mannitol, promotes fibrosis protein production. Ingenuity Pathway Analysis in the GSE database found that the mTOR, PKCδ, and NF-κB pathways were significantly changed during IVDD. The mTOR, PKCδ, and NF-κB inhibitors or siRNAs all abolished HG-induced fibrosis protein production. In addition, treatment of HAFCs with HG enhances the activation of mTOR, PKCδ, and NF-κB pathways. Thus, HG facilitates fibrosis in IVDD through mTOR, PKCδ, and NF-κB pathways. These results underscore the critical role of HG as a fibrotic factor in the progression of IVDD.

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Section: Discussionmentioning

confidence: 99%