ArticleCell death & disease2011
Celastrol inhibits aminoglycoside-induced ototoxicity via heat shock protein 32.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- Experimental and Clinical Approaches to Preventing Aminoglycoside-Induced Ototoxicity: A Scoping Review.Antioxidants (Basel, Switzerland) · 2025Review
- CORM‑2 reduces cisplatin accumulation in the mouse inner ear and protects against cisplatin-induced ototoxicity.Journal of advanced research · 2024Article
- Age-related hearing loss and its potential drug candidates: a systematic review.Chinese medicine · 2023Review
- Medical Therapy of Hearing Impairment and Tinnitus with Chinese Medicine: An Overview.Chinese journal of integrative medicine · 2023Review
- Sex differences in hearing impairment due to diet-induced obesity in CBA/Ca mice.Biology of sex differences · 2023Article
- The Role of Extracellular Vesicles in Diseases of the Ear, Nose, and Throat.Medical sciences (Basel, Switzerland) · 2022Review
- Hippo/YAP signaling pathway protects against neomycin-induced hair cell damage in the mouse cochlea.Cellular and molecular life sciences : CMLS · 2022Article
- Heme Oxygenase-1 Protects Hair Cells From Gentamicin-Induced Death.Frontiers in cellular neuroscience · 2022Article
- Progress in protecting vestibular hair cells.Archives of toxicology · 2021Review
- Review
- Exosome-mediated protection of auditory hair cells from ototoxic insults.The Journal of clinical investigation · 2020Article
- Exosomes mediate sensory hair cell protection in the inner ear.The Journal of clinical investigation · 2020Article
- Lovastatin protects against cisplatin-induced hearing loss in mice.Hearing research · 2020Article
- Hsp70/Bmi1-FoxO1-SOD Signaling Pathway Contributes to the Protective Effect of Sound Conditioning against Acute Acoustic Trauma in a Rat Model.Neural plasticity · 2020Article
- Cell-Specific Transcriptional Responses to Heat Shock in the Mouse Utricle Epithelium.Frontiers in cellular neuroscience · 2020Article
- Interactions between Macrophages and the Sensory Cells of the Inner Ear.Cold Spring Harbor perspectives in medicine · 2019Review
- Interleukin-17D and Nrf2 mediate initial innate immune cell recruitment and restrict MCMV infection.Scientific reports · 2018Article
- Celastrol enhances Atoh1 expression in inner ear stem cells and promotes their differentiation into functional auditory neuronal-like cells.Organogenesis · 2018Article
- The Inner Ear Heat Shock Transcriptional Signature Identifies Compounds That Protect Against Aminoglycoside Ototoxicity.Frontiers in cellular neuroscience · 2018Article
- Cisplatin Alters Antitumor Immunity and Synergizes with PD-1/PD-L1 Inhibition in Head and Neck Squamous Cell Carcinoma.Cancer immunology research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hearing loss is often caused by death of the mechanosensory hair cells of the inner ear. Hair cells are susceptible to death caused by aging, noise trauma, and ototoxic drugs, including the aminoglycoside antibiotics and the antineoplastic agent cisplatin. Ototoxic drugs result in permanent hearing loss for over 500,000 Americans annually. We showed previously that induction of heat shock proteins (HSPs) inhibits both aminoglycoside- and cisplatin-induced hair cell death in whole-organ cultures of utricles from adult mice. In order to begin to translate these findings into a clinical therapy aimed at inhibiting ototoxic drug-induced hearing loss, we have now examined a pharmacological HSP inducer, celastrol. Celastrol induced upregulation of HSPs in utricles, and it provided significant protection against aminoglycoside-induced hair cell death in vitro and in vivo. Moreover, celastrol inhibited hearing loss in mice receiving systemic aminoglycoside treatment. Our data indicate that the major heat shock transcription factor HSF-1 is not required for celastrol-mediated protection. HSP32 (also called heme oxygenase-1, HO-1) is the primary mediator of the protective effect of celastrol. HSP32/HO-1 inhibits pro-apoptotic c-Jun N-terminal kinase (JNK) activation and hair cell death. Taken together, our data indicate that celastrol inhibits aminoglycoside ototoxicity via HSP32/HO-1 induction.
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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.