ArticleCell death & disease2015
Loss of STAT1 protects hair cells from ototoxicity through modulation of STAT3, c-Jun, Akt, and autophagy factors.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- The Chemoprotective Potentials of Alpha-lipoic Acid against Cisplatin-induced Ototoxicity: A Systematic Review.Current medicinal chemistry · 2024Pooled it
- Pharmacologic Inhibition of JAK1/2 Potentiates Aminoglycoside-Induced Ototoxicity.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2026Article
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- Early downregulation of hair cell (HC)-specific genes in the vestibular sensory epithelium during chronic ototoxicity.Journal of biomedical science · 2025Article
- Mitochondrial-derived peptides, HNG and SHLP3, protect cochlear hair cells against gentamicin.Cell death discovery · 2024Article
- Advances in the Study of Etiology and Molecular Mechanisms of Sensorineural Hearing Loss.Cell biochemistry and biophysics · 2024Review
- Triethylene Glycol Squalene Improves Hair Regeneration by Maintaining the Inductive Capacity of Human Dermal Papilla Cells and Preventing Premature Aging.ACS pharmacology & translational science · 2024Article
- Molecular Specializations Underlying Phenotypic Differences in Inner Ear Hair Cells of Zebrafish and Mice.bioRxiv : the preprint server for biology · 2024Article
- Inhibition of autophagosome-lysosome fusion contributes to TDCIPP-induced Aβ1-42 production in N2a-APPswe cells.Heliyon · 2024Article
- SLC25A17 inhibits autophagy to promote triple-negative breast cancer tumorigenesis by ROS-mediated JAK2/STAT3 signaling pathway.Cancer cell international · 2024Article
- CRISPR/Cas9-mediated knockout of STAT1 in porcine-derived cell lines to elucidate the role of STAT1 in autophagy following classical swine fever virus infection.Frontiers in immunology · 2024Article
- Molecular specializations underlying phenotypic differences in inner ear hair cells of zebrafish and mice.Frontiers in neurology · 2024Article
- Molecular Characteristics of Cisplatin-Induced Ototoxicity and Therapeutic Interventions.International journal of molecular sciences · 2023Review
- Apelin-13 protects against cisplatin-induced ototoxicity by inhibiting apoptosis and regulating STAT1 and STAT3.Archives of toxicology · 2023Article
- PTEN inhibitor bisperoxovanadium protects against noise-induced hearing loss.Neural regeneration research · 2023Article
- YTHDF1 Protects Auditory Hair Cells from Cisplatin-Induced Damage by Activating Autophagy via the Promotion of ATG14 Translation.Molecular neurobiology · 2022Article
- The role of autophagy and ferroptosis in sensorineural hearing loss.Frontiers in neuroscience · 2022Review
- Oxidative Stress and Inflammation Caused by Cisplatin Ototoxicity.Antioxidants (Basel, Switzerland) · 2021Review
- Lmo4 Deficiency Enhances Susceptibility to Cisplatin-Induced Cochlear Apoptosis and Hearing Loss.Molecular neurobiology · 2021Article
- A Screen of Autophagy Compounds Implicates the Proteasome in Mammalian Aminoglycoside-Induced Hair Cell Damage.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hair cell damage is a side effect of cisplatin and aminoglycoside use. The inhibition or attenuation of this process is a target of many investigations. There is growing evidence that STAT1 deficiency decreases cisplatin-mediated ototoxicity; however, the role of STAT function and the molecules that act in gentamicin-mediated toxicity have not been fully elucidated. We used mice lacking STAT1 to investigate the effect of STAT1 ablation in cultured organs treated with cisplatin and gentamicin. Here we show that ablation of STAT1 decreased cisplatin toxicity and attenuated gentamicin-mediated hair cell damage. More TUNEL-positive hair cells were observed in explants of wild-type mice than that of STAT1(-/-) mice. Although cisplatin increased serine phosphorylation of STAT1 in wild-type mice and diminished STAT3 expression in wild-type and STAT1(-/-) mice, gentamicin increased tyrosine phosphorylation of STAT3 in STAT1(-/-) mice. The early inflammatory response was manifested in the upregulation of TNF-α and IL-6 in cisplatin-treated explants of wild-type and STAT1(-/-) mice. Expression of the anti-inflammatory cytokine IL-10 was altered in cisplatin-treated explants, upregulated in wild-type explants, and downregulated in STAT1(-/-) explants. Cisplatin and gentamicin triggered the activation of c-Jun. Activation of Akt was observed in gentamicin-treated explants from STAT1(-/-) mice. Increased levels of the autophagy proteins Beclin-1 and LC3-II were observed in STAT1(-/-) explants. These data suggest that STAT1 is a central player in mediating ototoxicity. Gentamicin and cisplatin activate different downstream factors to trigger ototoxicity. Although cisplatin and gentamicin triggered inflammation and activated apoptotic factors, the absence of STAT1 allowed the cells to overcome the effects of these drugs.
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