ArticleMolecular therapy. Nucleic acids2017
Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2.
Article in Molecular therapy. Nucleic acids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Metabolic and circadian inputs encode anticipatory biogenesis of hepatic fed microRNAs.Life science alliance · 2024Article
- Prenatal THC exposure induces long-term, sex-dependent cognitive dysfunction associated with lipidomic and neuronal pathology in the prefrontal cortex-hippocampal network.Molecular psychiatry · 2023Article
- Transcriptional Regulation of gga-miR-451 by AhR:Arnt inInternational journal of molecular sciences · 2019Article
- Deletion of miR-126a Promotes Hepatic Aging and Inflammation in a Mouse Model of Cholestasis.Molecular therapy. Nucleic acids · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Widely varied compounds, including certain plasticizers, hypolipidemic drugs (e.g., ciprofibrate, fenofibrate, WY-14643, and clofibrate), agrochemicals, and environmental pollutants, are peroxisome proliferators (PPs). Appropriate dose of PPs causes a moderate increase in the number and size of peroxisomes and the expression of genes encoding peroxisomal lipid-metabolizing enzymes. However, high-dose PPs cause varied harmful effects. Chronic administration of PPs to mice and rats results in hepatomegaly and ultimately carcinogenesis. Nuclear receptor protein peroxisome proliferator-activated receptor-α (Pparα) was shown to be required for this process. However, biological adaptations to minimize this risk are poorly understood. In this study, we found that miR-181a2 expression was induced by the Pparα agonist WY-14643. Moreover, exogenous expression of miR-181a-5p dramatically alleviated the cell toxicity caused by overactivation of Pparα. Further studies showed that miR-181a-5p directly targeted the Pparα 3' untranslated region and depressed the Pparα protein level. This study identified a feedback loop between miR-181a-5p and Pparα, which allows biological systems to approach a balance when Pparα is overactivated.
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Registered trials
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