ArticleNeurobiology of disease2013
Estrogen receptor β ligand therapy activates PI3K/Akt/mTOR signaling in oligodendrocytes and promotes remyelination in a mouse model of multiple sclerosis.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 117 citations in OpenAlex.
- Decoding the PI3K/Akt/mTOR-JAK/STAT signaling axis in multiple sclerosis: mechanistic crosstalk and therapeutic opportunities.Immunologic research · 2026Review
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Chloroindazole based estrogen receptor β ligands with favorable pharmacokinetics promote functional remyelination and visual recovery.Scientific reports · 2025Article
- Decreased mitochondrial activity in the demyelinating cerebellum of progressive multiple sclerosis and chronic EAE contributes to Purkinje cell loss.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of SIRT1 in Potentially Toxic Trace Elements (Lead, Fluoride, Aluminum and Cadmium) Associated Neurodevelopmental Toxicity.Biological trace element research · 2024Review
- The Importance of Phosphoinositide 3-Kinase in Neuroinflammation.International journal of molecular sciences · 2024Review
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- Article
- Neuroprotection in Cerebral Cortex Induced by the Pregnancy Hormone Estriol.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Matrine exerts its neuroprotective effects by modulating multiple neuronal pathways.Metabolic brain disease · 2023Review
- Signaling mechanisms involved in the regulation of remyelination in multiple sclerosis: a mini review.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Therapeutic modulation of JAK-STAT, mTOR, and PPAR-γ signaling in neurological dysfunctions.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Zebrafish as an emerging model to study estrogen receptors in neural development.Frontiers in endocrinology · 2023Review
- Hormonal Agents for the Treatment of Depression Associated with the Menopause.Drugs & aging · 2022Review
- Nuclear hormone receptors in demyelinating diseases.Journal of neuroendocrinology · 2022Review
- Human-Induced Pluripotent Stem Cell-Based Models for Studying Sex-Specific Differences in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2022Review
- Targeting the non-classical estrogen pathway in neurodegenerative diseases and brain injury disorders.Frontiers in endocrinology · 2022Review
- The effects of Korean Red Ginseng-derived components on oligodendrocyte lineage cells: Distinct facilitatory roles of the non-saponin and saponin fractions, and Rb1, in proliferation, differentiation and myelination.Journal of ginseng research · 2022Article
- Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells.Nutrients · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The identification of a drug that stimulates endogenous myelination and spares axon degeneration during multiple sclerosis (MS) could potentially reduce the rate of disease progression. Using experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, we have previously shown that prophylactic administration of the estrogen receptor (ER) β ligand 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) decreases clinical disease, is neuroprotective, stimulates endogenous myelination, and improves axon conduction without altering peripheral cytokine production or reducing central nervous system (CNS) inflammation. Here, we assessed the effects of therapeutic DPN treatment during peak EAE disease, which represents a more clinically relevant treatment paradigm. In addition, we investigated the mechanism of action of DPN treatment-induced recovery during EAE. Given that prophylactic and therapeutic treatments with DPN during EAE improved remyelination-induced axon conduction, and that ER (α and β) and membrane (m)ERs are present on oligodendrocyte lineage cells, a direct effect of treatment on oligodendrocytes is likely. DPN treatment of EAE animals resulted in phosphorylated ERβ and activated the phosphatidylinositol 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, a pathway required for oligodendrocyte survival and axon myelination. These results, along with our previous studies of prophylactic DPN treatment, make DPN and similar ERβ ligands immediate and favorable therapeutic candidates for demyelinating disease.
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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.