ArticlePloS one2017
Effects of peroxisome proliferator activated receptors (PPAR)-γ and -α agonists on cochlear protection from oxidative stress.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- PGC-1α and PPARs cooperatively mediate photoreceptor neuroprotection in rd1 mouse inherited retinal degeneration.Cell death & disease · 2026Article
- PFAS exposure induces hearing loss by targeting cochlear hair cells and spiral ganglion neurons.Scientific reports · 2026Article
- Unraveling Endocannabinoid Signaling Pathways in Cisplatin-Induced Ototoxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Network-Based Identification ofCurrent pharmaceutical design · 2026Article
- PFAS Exposure Induces Hearing Loss by Targeting Cochlear Hair Cells, Ribbon Synapses, and Spiral Ganglions.Research square · 2025Article
- Acquired sensorineural hearing loss, oxidative stress, and microRNAs.Neural regeneration research · 2025Article
- An In Vitro Oxidative Stress Model of the Human Inner Ear Using Human-Induced Pluripotent Stem Cell-Derived Otic Progenitor Cells.Antioxidants (Basel, Switzerland) · 2024Article
- L-Ergothioneine slows the progression of age-related hearing loss in CBA/CaJ mice.Hearing research · 2024Article
- Association of the protective effect of telmisartan on hearing loss among patients with hypertension.Frontiers in neurology · 2024Article
- Long-term NAD+ supplementation prevents the progression of age-related hearing loss in mice.Aging cell · 2023Article
- Fenofibrate attenuates the cytotoxic effect of cisplatin on lung cancer cells by enhancing the antioxidant defense systemOncology letters · 2023Article
- PPARα activator irbesartan suppresses the proliferation of endometrial carcinoma cells via SREBP1 and ARID1A.Oncology research · 2023Article
- Current Concepts and Future Trends in Increasing the Benefits of Cochlear Implantation: A Narrative Review.Medicina (Kaunas, Lithuania) · 2022Review
- Regulation of Neuroinflammatory Signaling by PPARγ Agonist in Mouse Model of Diabetes.International journal of molecular sciences · 2022Article
- Novel Application of Eupatilin for Effectively Attenuating Cisplatin-Induced Auditory Hair Cell Death via Mitochondrial Apoptosis Pathway.Oxidative medicine and cellular longevity · 2022Article
- Article
- Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats.International journal of molecular sciences · 2021Article
- Noise-Induced Cochlear Damage Involves PPAR Down-Regulation through the Interplay between Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2021Article
- The role of PPARγ in chemotherapy-evoked pain.Neuroscience letters · 2021Review
- Improving the Understanding of the Immunopathogenesis of Lymphopenia as a Correlate of SARS-CoV-2 Infection Risk and Disease Progression in African Patients: Protocol for a Cross-sectional Study.JMIR research protocols · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various insults cause ototoxicity in mammals by increasing oxidative stress leading to apoptosis of auditory hair cells (HCs). The thiazolidinediones (TZDs; e.g., pioglitazone) and fibrate (e.g., fenofibrate) drugs are used for the treatment of diabetes and dyslipidemia. These agents target the peroxisome proliferator-activated receptors, PPARγ and PPARα, which are transcription factors that influence glucose and lipid metabolism, inflammation, and organ protection. In this study, we explored the effects of pioglitazone and other PPAR agonists to prevent gentamicin-induced oxidative stress and apoptosis in mouse organ of Corti (OC) explants. Western blots showed high levels of PPARγ and PPARα proteins in mouse OC lysates. Immunofluorescence assays indicated that PPARγ and PPARα proteins are present in auditory HCs and other cell types in the mouse cochlea. Gentamicin treatment induced production of reactive oxygen species (ROS), lipid peroxidation, caspase activation, PARP-1 cleavage, and HC apoptosis in cultured OCs. Pioglitazone mediated its anti-apoptotic effects by opposing the increase in ROS induced by gentamicin, which inhibited the subsequent formation of 4-hydroxy-2-nonenal (4-HNE) and activation of pro-apoptotic mediators. Pioglitazone mediated its effects by upregulating genes that control ROS production and detoxification pathways leading to restoration of the reduced:oxidized glutathione ratio. Structurally diverse PPAR agonists were protective of HCs. Pioglitazone (PPARγ-specific), tesaglitazar (PPARγ/α-specific), and fenofibric acid (PPARα-specific) all provided >90% protection from gentamicin toxicity by regulation of overlapping subsets of genes controlling ROS detoxification. This study revealed that PPARs play important roles in the cochlea, and that PPAR-targeting drugs possess therapeutic potential as treatment for hearing loss.
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