ReviewNeurobiology of disease2021
Epigenetic regulators of neuronal ferroptosis identify novel therapeutics for neurological diseases: HDACs, transglutaminases, and HIF prolyl hydroxylases.
Review in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- H3K14 lactylation exacerbates neuronal ferroptosis by inhibiting calcium efflux following intracerebral hemorrhagic stroke.Cell death & disease · 2025Article
- Exploring the active ingredients and potential mechanisms of Pingchan granules in Parkinson's disease treatment through network pharmacology and transcriptomics.Scientific reports · 2025Article
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Article
- Pharmacological inhibition of astrocytic transglutaminase 2 facilitates the expression of a neurosupportive astrocyte reactive phenotype in association with increased histone acetylation.bioRxiv : the preprint server for biology · 2024Article
- Tellurium-Doped Bioactive Glass Induces Ferroptosis in Osteosarcoma Cells Regardless of FSP1.Antioxidants (Basel, Switzerland) · 2024Article
- Molecular Determinants for Photodynamic Therapy Resistance and Improved Photosensitizer Delivery in Glioma.International journal of molecular sciences · 2024Review
- Molecular subtype identification of cerebral ischemic stroke based on ferroptosis-related genes.Scientific reports · 2024Article
- Attenuation of neuronal ferroptosis in intracerebral hemorrhage by inhibiting HDAC1/2: Microglial heterogenization via the Nrf2/HO1 pathway.CNS neuroscience & therapeutics · 2024Article
- Emerging roles and therapeutic potentials of ferroptosis: from the perspective of 11 human body organ systems.Molecular and cellular biochemistry · 2023Review
- Article
- Epigenetic Regulation of Ferroptosis in Central Nervous System Diseases.Molecular neurobiology · 2023Review
- Type 2 transglutaminase in the nucleus: the new epigenetic face of a cytoplasmic enzyme.Cellular and molecular life sciences : CMLS · 2023Review
- Exploring links between 2-oxoglutarate-dependent oxygenases and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Review
- First-in-Class Dual Mechanism Ferroptosis-HDAC Inhibitor Hybrids.Journal of medicinal chemistry · 2022Article
- Article
- Iron Transporters and Ferroptosis in Malignant Brain Tumors.Frontiers in oncology · 2022Review
- Ferroptosis Induction in Multiple Myeloma Cells Triggers DNA Methylation and Histone Modification Changes Associated with Cellular Senescence.International journal of molecular sciences · 2021Article
- Novel Histone Deacetylase Inhibitors for Treating HIV Infection.ACS medicinal chemistry letters · 2021Article
- Novel Histone Deacetylase 6 Inhibitors for Treating Alzheimer's Disease and Cancer.ACS medicinal chemistry letters · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
A major thrust of our laboratory has been to identify how physiological stress is transduced into transcriptional responses that feed back to overcome the inciting stress or its consequences, thereby fostering survival and repair. To this end, we have adopted the use of an in vitro model of ferroptosis, a caspase-independent, but iron-dependent form of cell death (Dixon et al., 2012; Ratan, 2020). In this review, we highlight three distinct epigenetic targets that have evolved from our studies and which have been validated in vivo studies. In the first section, we discuss our studies of broad, pan-selective histone deacetylase (HDAC) inhibitors in ferroptosis and how these studies led to the validation of HDAC inhibitors as candidate therapeutics in a host of disease models. In the second section, we discuss our studies that revealed a role for transglutaminase as an epigenetic modulator of proferroptotic pathways and how these studies set the stage for recent elucidation of monoamines as post-translation modifiers of histone function. In the final section, we discuss our studies of iron-, 2-oxoglutarate-, and oxygen-dependent dioxygenases and the role of one family of these enzymes, the HIF prolyl hydroxylases, in mediating transcriptional events necessary for ferroptosis in vitro and for dysfunction in a host of neurological conditions. Overall, our studies highlight the importance of epigenetic proteins in mediating prodeath and prosurvival responses to ferroptosis. Pharmacological agents that target these epigenetic proteins are showing robust beneficial effects in diverse rodent models of stroke, Parkinson's disease, Huntington's disease, and Alzheimer's disease.
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