Evidence map›Paper›PMID 30600476›Full record

ReviewNeuromolecular medicine2019

The Emerging Roles of Ferroptosis in Huntington's Disease.

Yajing Mi, Xingchun Gao, Hao Xu, Yuanyuan Cui, Yuelin Zhang, Xingchun Gou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Impact of Oxidative Stress-Driven Ferroptosis in Neurodegeneration.International journal of molecular sciences · 2026
    Review
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5 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Yajing MiShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China.
Xingchun GaoShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China.
Hao XuShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China.
Yuanyuan CuiShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China.
Yuelin ZhangShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China. zhangyuelin68@163.com.
Xingchun GouShaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China. gouxingchun@189.cn.
Xi'an Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal dominant and fatal neurodegenerative disorder, which is caused by an abnormal CAG repeat in the huntingtin gene. Despite its well-defined genetic origin, the molecular mechanisms of neuronal death are unclear yet, thus there are no effective strategies to block or postpone the process of HD. Ferroptosis, a recently identified iron-dependent cell death, attracts considerable attention due to its putative involvement in neurodegenerative diseases. Accumulative data suggest that ferroptosis is very likely to participate in HD, and inhibition of the molecules and signaling pathways involved in ferroptosis can significantly eliminate the symptoms and pathology of HD. This review first describes evidence for the close relevance of ferroptosis and HD in patients and mouse models, then summarizes advances for the mechanisms of ferroptosis involved in HD, finally outlines some therapeutic strategies targeted ferroptosis. Comprehensive understanding of the emerging roles of ferroptosis in the occurrence of HD will help us to explore effective therapies for slowing the progression of this disease.

Indexed as

FerroptosisAnimalsAntioxidantsDisease Models, AnimalHumansHuntingtin ProteinHuntington DiseaseIronIron Chelating AgentsLipid PeroxidationMiceMice, TransgenicNeurogliaNeuronsNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidaseAntioxidantsglutathione peroxidase 4, mouseHTT protein, humanHtt protein, mouseHuntingtin ProteinIronIron Chelating AgentsNFE2L2 protein, humanNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidaseFerroptosisHuntington’s diseaseIron accumulationLipid peroxidationMutant Huntingtin

Identifiers

PMID30600476
OpenAlexW2907074026

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.