Evidence map›Paper›PMID 34445125›Full record

ArticleInternational journal of molecular sciences2021

miR-302 Attenuates Mutant Huntingtin-Induced Cytotoxicity through Restoration of Autophagy and Insulin Sensitivity.

Ching-Chi Chang, Sing-Hua Tsou, Wei-Jen Chen, Ying-Jui Ho, Hui-Chih Hung, Guang-Yaw Liu, Sandeep Kumar Singh, Hsin-Hua Li, Chih-Li Lin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  4. Observational
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  7. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Ching-Chi ChangDepartment of Psychiatry, Chung Shan Medical University Hospital, Taichung 402, Taiwan.ORCID 0000-0002-6081-9152
Sing-Hua TsouInstitute of Medicine, College of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.ORCID 0000-0001-7574-028X
Wei-Jen ChenDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung 402, Taiwan.ORCID 0000-0002-3729-989X
Ying-Jui HoDepartment of Psychology, Chung Shan Medical University, Taichung 402, Taiwan.
Hui-Chih HungDepartment of Life Sciences, Institute of Genomics and Bioinformatics, National Chung Hsing University, Taichung 402, Taiwan.ORCID 0000-0003-0180-1822
Guang-Yaw LiuInstitute of Medicine, College of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Sandeep Kumar SinghIndian Scientific Education and Technology Foundation, Lucknow 226002, India.ORCID 0000-0002-0022-6240
Hsin-Hua LiInstitute of Medicine, College of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Chih-Li LinInstitute of Medicine, College of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.ORCID 0000-0003-4553-3727
Chung Shan Medical University · TWChung Shan Medical University Hospital · TWNational Chung Hsing University · TWUnited States India Educational Foundation · IN

Funding

Chung Shan Medical University Hospital CSH-2018-C-003Ministry of Science and Technology 108-2320-B-040-029-MY2, 108-2314-B-040-023-MY3, 109-2320-B-040-021the bilateral project from National Chung Hsing University and Chung Shan Medical University NCHU-CSMU-10901
6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal-dominant brain disorder caused by mutant huntingtin (mHtt). Although the detailed mechanisms remain unclear, the mutational expansion of polyglutamine in mHtt is proposed to induce protein aggregates and neuronal toxicity. Previous studies have shown that the decreased insulin sensitivity is closely related to mHtt-associated impairments in HD patients. However, how mHtt interferes with insulin signaling in neurons is still unknown. In the present study, we used a HD cell model to demonstrate that the miR-302 cluster, an embryonic stem cell-specific polycistronic miRNA, is significantly downregulated in mHtt-Q74-overexpressing neuronal cells. On the contrary, restoration of miR-302 cluster was shown to attenuate mHtt-induced cytotoxicity by improving insulin sensitivity, leading to a reduction of mHtt aggregates through the enhancement of autophagy. In addition, miR-302 also promoted mitophagy and stimulated Sirt1/AMPK-PGC1α pathway thereby preserving mitochondrial function. Taken together, these results highlight the potential role of miR-302 cluster in neuronal cells, and provide a novel mechanism for mHtt-impaired insulin signaling in the pathogenesis of HD.

Indexed as

AutophagyCells, CulturedDown-RegulationEmbryonic Stem CellsHumansHuntingtin ProteinHuntington DiseaseInsulinInsulin ResistanceMicroRNAsMitochondriaMitophagyNeuronsSignal TransductionHTT protein, humanHuntingtin ProteinInsulinMicroRNAsMIRN302A microRNA, humanautophagyHuntington’s diseaseinsulin signalingmiR-302mitophagy

Identifiers

PMID34445125
PMCPMC8395150
OpenAlexW3193266787

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.