ArticleLife science alliance2024
Nr1h4 and Thrb ameliorate ER stress and provide protection in the MPTP mouse model of Parkinson's.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Taurochenodeoxycholic acid alleviates MPPIBRO neuroscience reports · 2026Article
- Hypoxia and TTR dysregulation in astrocytes from Parkinson's disease with a specific mitochondrial haplogroup: A single-cell analysis.Neural regeneration research · 2026Article
- Integrated approaches to target nuclear receptors for managing the co-morbidity of tuberculosis and diabetes.Frontiers in immunology · 2026Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated ER stress has been linked to the pathogenesis of several disease conditions including neurodegeneration. In this study, we have holistically determined the differential expression of all the nuclear receptors (NRs) in the presence of classical ER stress inducers. Activation of Nr1h4 and Thrb by their cognate ligands (GW4064 and T3) ameliorates the tunicamycin (TM)-induced expression of ER stress genes. A combination of both ligands is effective in mitigating cell death induced by TM. Further exploration of their protective effects in the Parkinson's disease (PD) model shows that they reduce MPP
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