ArticleRedox biology2020
The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 162 citations in OpenAlex.
- Cordycepin Alleviates Acute Lung Injury by Targeting TAK1 to Inhibit MAPK and NF-κB Signaling Pathways.Biomolecules · 2026Article
- Inflammatory Signatures of Tinnitus in Patients and Mice.Neuroscience bulletin · 2026Article
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- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- ATG5-FOXA3 Axis Contributes to Lysosomal Biogenesis and Auditory Function in Kölliker's Organ.Biomedicines · 2026Article
- Superenhancer-mediated ferroptosis in age-related hearing loss: cochlear epigenomics.Cellular and molecular life sciences : CMLS · 2026Article
- Mitophagy Activation by N-Acetylcysteine Protects against Mic60 Deficiency-Induced Auditory Neuropathy.Neuroscience bulletin · 2026Article
- XIAP Stabilizes DDRGK1 to Promote ER-Phagy and Protects Against Noise-Induced Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Autophagy for Otoprotection: Translating Basic Mechanisms into Clinical Strategies.International journal of molecular sciences · 2026Review
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip.Journal of advanced research · 2026Article
- Article
- The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss.Frontiers in molecular neuroscience · 2026Article
- Liposome-Encapsulated Rutin Attenuates Cisplatin-Induced Ototoxicity via Suppression of P53-Associated Oxidative Injury.Biomaterials research · 2026Article
- DNA methylation signatures of frailty beyond age: a longitudinal study of female and male mice.bioRxiv : the preprint server for biology · 2025Article
- miR-101/METTL3 axis induces autophagy by interrupting FOXG1/EIF3J-AS1 binding in gliomas.Cell death & disease · 2025Article
- Comparative Cochlear Transcriptomics in Echolocating Bats and Mouse Reveals Hras as Protector Against Noise-Induced Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting NLRP3/caspase-1/GSDMD to treat inner ear injury from labyrinthine hemorrhage.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Pinoresinol Diglucoside Attenuates Nuclear Receptor Coactivator 4-Mediated Ferritinophagy Associated with Cisplatin-Induced Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a self-defense response to protect individuals from infection and tissue damage, but excessive or persistent inflammation can have adverse effects on cell survival. Many individuals become especially susceptible to chronic-inflammation-induced sensorineural hearing loss as they age, but the intrinsic molecular mechanism behind aging individuals' increased risk of hearing loss remains unclear. FoxG1 (forkhead box transcription factor G1) is a key transcription factor that plays important roles in hair cell survival through the regulation of mitochondrial function, but how the function of FoxG1 changes during aging and under inflammatory conditions is unknown. In this study, we first found that FoxG1 expression and autophagy both increased gradually in the low concentration lipopolysaccharide (LPS)-induced inflammation model, while after high concentration of LPS treatment both FoxG1 expression and autophagy levels decreased as the concentration of LPS increased. We then used siRNA to downregulate Foxg1 expression in hair cell-like OC-1 cells and found that cell death and apoptosis were significantly increased after LPS injury. Furthermore, we used d-galactose (D-gal) to create an aging model with hair cell-like OC-1 cells and cochlear explant cultures in vitro and found that the expression of Foxg1 and the level of autophagy were both decreased after D-gal and LPS co-treatment. Lastly, we knocked down the expression of Foxg1 under aged inflammation conditions and found increased numbers of dead and apoptotic cells. Together these results suggest that FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.