Evidence map›Paper›PMID 33421017›Full record

ArticleMolecular neurobiology2021

Fibroblast Growth Factor 9 Stimulates Neuronal Length Through NF-kB Signaling in Striatal Cell Huntington's Disease Models.

Issa Olakunle Yusuf, Hsiu-Mei Chen, Pei-Hsun Cheng, Chih-Yi Chang, Shaw-Jenq Tsai, Jih-Ing Chuang, Chia-Ching Wu, Bu-Miin Huang, H Sunny Sun, Chuan-Mu Chen and 1 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 27% 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, 17 citations in OpenAlex.

  1. Review
  2. Wild-type C9orf72 drives proteasomal dysfunction and mutant aggregates via a Stat1-Isg15 axis in Huntington's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
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

11 authors at 5 institutions in 1 country.

Issa Olakunle Yusuf *Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Cheng Kung University and Academia Sinica, Taipei, 11529, Taiwan.
Hsiu-Mei Chen *Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Pei-Hsun ChengDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Chih-Yi ChangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Shaw-Jenq TsaiDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Jih-Ing ChuangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Chia-Ching WuInstitute of Basic Medical Sciences, Taipei, Taiwan.
Bu-Miin HuangInstitute of Basic Medical Sciences, Taipei, Taiwan.
H Sunny SunInstitute of Basic Medical Sciences, Taipei, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, College of Life Sciences, National Chung Hsing University, Taichung, 40227, Taiwan.
Shang-Hsun YangTaiwan International Graduate Program in Interdisciplinary Neuroscience, National Cheng Kung University and Academia Sinica, Taipei, 11529, Taiwan. syang@mail.ncku.edu.tw.ORCID http://orcid.org/0000-0002-1601-3653
Taipei Institute of Pathology · TWNational Cheng Kung University · TWMackay Junior College of Medicine, Nursing and Management · TWNational Chung Hsing University · TWTaipei Medical University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 105-2628-B-006-015-MY3, 108-2314-B-006 -079 -MY3 and MOST 106-2320-B-006-004
6 · The paper itself

Abstract

Proper development of neuronal cells is important for brain functions, and impairment of neuronal development may lead to neuronal disorders, implying that improvement in neuronal development may be a therapeutic direction for these diseases. Huntington's disease (HD) is a neurodegenerative disease characterized by impairment of neuronal structures, ultimately leading to neuronal death and dysfunctions of the central nervous system. Based on previous studies, fibroblast growth factor 9 (FGF9) may provide neuroprotective functions in HD, and FGFs may enhance neuronal development and neurite outgrowth. However, whether FGF9 can provide neuronal protective functions through improvement of neuronal morphology in HD is still unclear. Here, we study the effects of FGF9 on neuronal length in HD and attempt to understand the related working mechanisms. Taking advantage of striatal cell lines from HD knock-in mice, we found that FGF9 increases total neuronal length and upregulates several structural and synaptic proteins under HD conditions. In addition, activation of nuclear factor kappa B (NF-kB) signaling by FGF9 was observed to be significant in HD cells, and blockage of NF-kB leads to suppression of these structural and synaptic proteins induced by FGF9, suggesting the involvement of NF-kB signaling in these effects of FGF9. Taken these results together, FGF9 may enhance total neuronal length through upregulation of NF-kB signaling, and this mechanism could serve as an important mechanism for neuroprotective functions of FGF9 in HD.

Indexed as

AnimalsCell LineCorpus StriatumDisease Models, AnimalFibroblast Growth Factor 9Huntington DiseaseMiceNeuronal OutgrowthNeuronsNF-kappa BSignal TransductionUp-RegulationFibroblast Growth Factor 9NF-kappa BFibroblast growth factor 9Huntington’s diseaseNeuronal lengthNF-κB signaling

Identifiers

PMID33421017
OpenAlexW3118565083

What Socratic 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 Socratic graph.