ArticleCell death & disease2017
HDAC6 inhibition by tubastatin A is protective against oxidative stress in a photoreceptor cell line and restores visual function in a zebrafish model of inherited blindness.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Intravitreal Administration of a Selective HDAC6 Inhibitor Prevents Retinal Damage Progression in the Acute Ocular Toxoplasmosis Model.ACS infectious diseases · 2026Article
- A real-world pharmacovigilance study of romidepsin based on FDA adverse event reporting system database.Frontiers in oncology · 2026Article
- Therapeutic potential of HDAC6 inhibitor Tubastatin A in health and diseases: current perspective and future directions.Military Medical Research · 2026Review
- Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).International journal of molecular medicine · 2025Review
- Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- A review of the 661W cell line as a tool to facilitate treatment development for retinal diseases.Cell & bioscience · 2025Review
- Uncovering Novel Drugs that Restore Vision Using Orthogonal Pooling in Zebrafish.Advances in experimental medicine and biology · 2025Article
- MAPK8 and HDAC6: potential biomarkers related to autophagy in diabetic retinopathy based on bioinformatics analysis.Frontiers in endocrinology · 2025Article
- Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.Results and problems in cell differentiation · 2025Review
- Review
- Epigenetic Switches in Retinal Homeostasis and Target for Drug Development.International journal of molecular sciences · 2024Review
- Epidrugs as Promising Tools to EliminatePharmaceutics · 2023Article
- Acetylated α-tubulin alleviates injury to the dendritic spines after ischemic stroke in mice.CNS neuroscience & therapeutics · 2023Article
- Advances in the Mechanistic Study of the Control of Oxidative Stress Injury by Modulating HDAC6 Activity.Cell biochemistry and biophysics · 2023Article
- The role of epigenetic changes in the pathology and treatment of inherited retinal diseases.Frontiers in cell and developmental biology · 2023Review
- Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022Review
- Targeting the HDAC6-Cilium Axis Ameliorates the Pathological Changes Associated with Retinopathy of Prematurity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Upregulation of MDH1 acetylation by HDAC6 inhibition protects against oxidative stress-derived neuronal apoptosis following intracerebral hemorrhage.Cellular and molecular life sciences : CMLS · 2022Article
- Macrophage migration inhibitory factor (MIF) acetylation protects neurons from ischemic injury.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal diseases, such as hereditary retinitis pigmentosa and age-related macular degeneration, are characterized by the progressive loss of photoreceptors. Histone deacetylase 6 (HDAC6) is considered as a stress surveillance factor and a potential target for neuroprotection and regeneration. Overexpression of HDAC6 has been connected to neurodegenerative disorders, and its suppression may provide protection. Here we show that HDAC6 is constitutively present in the mouse retina, and in the cone-like mouse cell line 661W. In 661W cells HDAC6 inhibition by the specific inhibitor tubastatin A (TST) led to the acetylation of α-tubulin, which is a major substrate for HDAC6. After oxidative stress, exerted by hydrogen peroxide, TST promoted cell survival and the upregulation of heat-shock proteins HSP70 and HSP25 by activation of heat-shock transcription factor 1. Furthermore, in response to oxidative stress the redox regulatory protein peroxiredoxin 1 (Prx1) was modulated in 661W cells by HDAC6 inhibition. The peroxide reducing activity of Prx1 is dependent on its acetylation, which is mediated by HDAC6. Pre-incubation with TST prevented the inactivation of Prx1 and its preserved activity may exert protective effects in photoreceptor cells. To determine whether TST treatment has a therapeutic effect on visual function, the dye
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