ArticleJournal of cellular and molecular medicine2024
4-octyl itaconate alleviates cisplatin-induced ferroptosis possibly via activating the NRF2/HO-1 signalling pathway.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Article
- Licochalcone A mitigates cisplatin-induced nephrotoxicity by inhibiting ferroptosis and mitochondrial dysfunction via the Nrf2/GPX4 axis.Frontiers in pharmacology · 2026Article
- Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Antioxidant Intervention Against Microplastic Hazards.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting Programmed Cell Death in Acquired Sensorineural Hearing Loss: Ferroptosis, Necroptosis, and Pyroptosis.Neuroscience bulletin · 2025Review
- Protective effects of indole-3-propionic acid against TCP-induced hearing loss in mice by mitigating oxidative stress and promoting neutrophil recruitment.Scientific reports · 2025Article
- Sarsasapogenin protects hair cells from cisplatin-induced ototoxicity by attenuating apoptosis and ferroptosis via alleviating oxidative stress.Frontiers in pharmacology · 2025Article
- Targeting Ferroptosis: Small-molecule Inducers as Novel Anticancer Agents.Anti-cancer agents in medicinal chemistry · 2025Review
- Cisplatin-Induced Hearing Loss, Oxidative Stress, and Antioxidants as a Therapeutic Strategy-A State-of-the-Art Review.Antioxidants (Basel, Switzerland) · 2024Review
- [Experimental study on promotion of peripheral nerve regeneration by selenium-methylselenocysteine].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- 4-octyl itaconate alleviates cisplatin-induced ferroptosis possibly via activating the NRF2/HO-1 signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Apoptosis, autophagy, ferroptosis, and pyroptosis in cisplatin-induced ototoxicity and protective agents.Frontiers in pharmacology · 2024Review
- Targeting ferroptosis in sensorineural hearing loss: mechanisms, therapeutics, and translational prospects.Frontiers in neurologyReview
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Ferroptosis, characterized by iron-dependent lipid reactive oxygen species (ROS) accumulation, plays a pivotal role in cisplatin-induced ototoxicity. Existing research has suggested that in cisplatin-mediated damage to auditory cells and hearing loss, ferroptosis is partially implicated. 4-Octyl itaconate (4-OI), derived from itaconic acid, effectively permeates cell membranes, showcasing potent anti-inflammatory as well as antioxidant effects in several disease models. Our study aimed to investigate the effect of 4-OI on cisplatin-induced ferroptosis and the underlying molecular mechanisms. The survival rates of HEI-OC1 cells and mice cochlea hair cells were measured by CCK8 and immunofluorescence, respectively. The auditory brainstem response (ABR) audiometry was used to detect changes in hearing thresholds in mice before and after treatment. Levels of ROS were evaluated by DCFH-DA. Real-time PCR quantified inflammatory cytokines TNF-α, IL-6 and IL-1β. Network Pharmacology and RNA sequencing (RNA-seq) analysis of the potential mechanism of 4-OI resistance to cisplatin-induced ferroptosis. The expressions of ferroptosis-related factors (GPX4, SLC7A11 and PTGS2) and important antioxidant factors (NRF2, HO-1, GCLC and NQO1) were tested by real-time PCR, Western blot and immunofluorescence. Results demonstrated cisplatin-induced significant ROS and inflammatory factor release, reduced NRF2 expression, hindered nuclear translocation and activated ferroptosis. Pretreatment with 4-OI exhibited anti-inflammatory and antioxidant effects, along with resistance to ferroptosis, ultimately mitigating cisplatin-induced cell loss. In the present study, we show that 4-OI inhibits cisplatin-induced ferroptosis possibly through activation of the NRF2/HO-1 signalling pathway, thereby exerting a protective effect against cisplatin-induced damage to auditory cells, and providing a new therapeutic strategy for cisplatin-induced hearing loss.
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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.