ArticleMolecular neurobiology2020
All-Trans Retinoic Acid Exerts Neuroprotective Effects in Amyotrophic Lateral Sclerosis-Like Tg (SOD1*G93A)1Gur Mice.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Vitamin A retinoic acid contributes to muscle stem cell and mitochondrial function loss in old age.JCI insight · 2025Article
- The therapeutic potential of Apigenin in amyotrophic lateral sclerosis through ALDH1A2/Nrf2/ARE signaling.Molecular medicine (Cambridge, Mass.) · 2024Article
- Evaluation of a Synthetic Retinoid, Ellorarxine, in the NSC-34 Cell Model of Motor Neuron Disease.International journal of molecular sciences · 2024Article
- Article
- Neuroprotective effects of ellorarxine in neuronal models of degeneration.Frontiers in neuroscience · 2024Article
- EYE-503: A Novel Retinoic Acid Drug for Treating Retinal Neurodegeneration.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Circulating NAD+ Metabolism-Derived Genes Unveils Prognostic and Peripheral Immune Infiltration in Amyotrophic Lateral Sclerosis.Frontiers in cell and developmental biology · 2022Article
- Identification of Molecular Correlations Between DHRS4 and Progressive Neurodegeneration in Amyotrophic Lateral Sclerosis By Gene Co-Expression Network Analysis.Frontiers in immunology · 2022Article
- All-Trans Retinoic Acid Attenuates Blue Light-Induced Apoptosis of Retinal Photoreceptors by Upregulating MKP-1 Expression.Molecular neurobiology · 2021Article
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
All-trans retinoic acid (ATRA), a ligand of retinoic acid receptors, could regulate various biological processes by activating retinoic acid signals. Recent studies suggested that ATRA displays multiple neuroprotective effects and thereby alleviates the disease progression in a variety of neurological diseases. Our previous studies found that the impaired retinoic acid signal decreased ALDH1A2, an essential synthetase of ATRA, in the spinal cord of ALS mice. Here, we evaluated the neuroprotective and neurorestorative effects of ATRA in a SOD1-G93A transgenic mice model of ALS. We administrated ATRA(3 mg/kg) daily from the onset stage to the progression stage for 5 weeks. Behavioral tests showed that ATRA improved the forelimb grip strength in ALS mice and may slow the disease progression, but not the body weight. ATRA could completely reverse the impaired retinoic acid receptor alpha (RARα) signal in the spinal cord of ALS mice. This effect was accompanied by enhancing the degradation of misfolded proteins via the ubiquitin-proteasome system, regulating the oxidative stress, inhibiting the astrocyte activation, and promoting the neurotrophic signal recovery. Our findings are the first to indicate that the damaged retinoic acid signal is involved in the pathogenesis of ALS, and ATRA could induce the functional neuroprotection via repairing the damaged retinoic acid signal.
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