ArticleCell death & disease2017
P16INK4a upregulation mediated by TBK1 induces retinal ganglion cell senescence in ischemic injury.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- The Profile of Retinal Ganglion Cell Death and Cellular Senescence in Mice with Aging.International journal of molecular sciences · 2025Article
- PRMT5 Regulates Senescence in Retinal Ganglion Cells by Targeting the Wnt/β-Catenin Signaling Cascade.Investigative ophthalmology & visual science · 2025Article
- Tank-binding kinase 1 regulates inflammation and autophagy in glaucoma.Frontiers in neuroscience · 2025Review
- Targeting ATAD3A Phosphorylation Mediated by TBK1 Ameliorates Senescence-Associated Pathologies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Predicting Outcomes in Esophageal Squamous Cell Carcinoma Using scRNA-Seq and Bulk RNA-Seq: A Model Development and Validation Study.Cancer medicine · 2025Article
- Cellular senescence mediates retinal ganglion cell survival regulation post-optic nerve crush injury.Cell proliferation · 2024Article
- The Impact of Aging on Ocular Diseases: Unveiling Complex Interactions.Aging and disease · 2024Review
- SH-SY5Y human neuronal cells with mutations of theBiochemistry and biophysics reports · 2024Article
- Aging, Cellular Senescence, and Glaucoma.Aging and disease · 2024Review
- Reduced glutathione level in the aqueous humor of patients with primary open-angle glaucoma and normal-tension glaucoma.npj aging · 2023Article
- Markers of senescence are often associated with neuronal differentiation in the developing sensory systems.Histology and histopathology · 2023Review
- Covalent Organic Framework (COF): A Drug and Carrier to Attenuate Retinal Ganglion Cells Death in an Acute Glaucoma Mouse Model.Polymers · 2022Article
- Article
- Knockdown of TANK-Binding Kinase 1 Enhances the Sensitivity of Hepatocellular Carcinoma Cells to Molecular-Targeted Drugs.Frontiers in pharmacology · 2022Article
- Calcium channel ITPR2 and mitochondria-ER contacts promote cellular senescence and aging.Nature communications · 2021Article
- Is Senescence-Associated β-Galactosidase a ReliableFrontiers in cell and developmental biology · 2021Review
- Evaluating the neuroprotective impact of senolytic drugs on human vision.Scientific reports · 2020Article
- Article
- Early removal of senescent cells protects retinal ganglion cells loss in experimental ocular hypertension.Aging cell · 2020Article
- Molecular mechanisms of retinal ischemia.Current opinion in physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma is a leading cause of irreversible blindness worldwide that is characterized by progressive retinal ganglion cell (RGC) death. However, RGC senescence as a phase before RGC death, and the mechanism of RGC senescence remains unclear. Here, we demonstrate that TANK-binding protein 1 (TBK1) is upregulated in acute IOP elevation-induced ischemic retinas mouse model. Moreover, pre-treatment with the TBK1 inhibitor BX-795 reduced p16INK4a (p16) expression and RGC senescence. Upregulation of TBK1 via plasmid transfection increased Akt phosphorylation at Ser473 and Bmi1 phosphorylation. The Akt inhibitor MK-2206 decreased the expression of p16 and Bmi1 serine phosphorylation. A Bmi1 Ser316 mutation also attenuated TBK1-induced p16 upregulation. Finally, silencing of TBK1 via shRNA knockdown reduced the expression of p16 as well as Akt and Bmi1 phosphorylation, reducing RGC senescence in vivo. These data suggest that acute IOP elevation-induced ischemia increases TBK1 expression, which then increases p16 expression through the Akt- Bmi1 phosphorylation pathway. This study therefore elucidates a novel mechanism whereby TBK1 regulates p16 expression and RGC senescence, suggesting a potential novel treatment strategy for minimizing RGC senescence in retinal ischemia and glaucoma.
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