Evidence map›Paper›PMID 40713750›Full record

ArticleCell & bioscience2025

Insulin-like growth factor 2 reduces Huntington's disease aggregates via AKT and NF-κB signaling in huntington's disease.

Yun-Shiuan Tung, Chih-Wei Tung, Siew Chin Chan, Yi-Ching Chen, Po-Ming Wu, Pei-Hsun Cheng, Chuan-Mu Chen, Shang-Hsun Yang

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In one paragraph

Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  3. 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
  4. 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

8 authors.

Yun-Shiuan Tung *Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Chih-Wei Tung *Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Siew Chin Chan *Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Yi-Ching Chen *Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Po-Ming WuDepartment of Pediatrics, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, 70101, Taiwan.
Pei-Hsun ChengDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, College of Life Sciences, National Chung Hsing University, Taichung, 40227, Taiwan.
Shang-Hsun YangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. syang@mail.ncku.edu.tw.ORCID http://orcid.org/0000-0002-1601-3653

Funding

National Science and Technology Council 111-2320-B-006-035-MY3 and 111-2320-B-006-020-MY3
6 · The paper itself

Abstract

backgroundAggregation of misfolded mutant Huntingtin (mHTT) is a pathological characteristic in Huntington’s disease (HD), implying clearance of mHTT is a therapeutical direction for this neurodegenerative disorder. Based on previous studies, Insulin-like growth factor 2 (IGF2) enhances microfilament polymerization in HD models; however, the role of IGF2 against mHTT aggregates is still unclear.

resultsHere, we demonstrate that IGF2 expression is significantly lower in symptomatic HD patients compared to presymptomatic individuals, and IGF2 activation mechanistically enhances phosphorylation of Protein Kinase B(AKT; serine/threonine kinase), which subsequently reduces mHTT aggregates in vitro. Furthermore, IGF2 stimulates Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, promoting the secretion of mHTT within extracellular vesicles, thereby aiding cellular clearance. In vivo studies in R6/2 HD transgenic mice reveal that IGF2 administration improves motor functions and decreases mHTT levels.

conclusionsCollectively, our findings elucidate the multifaceted role of IGF2 in HD, highlighting its therapeutic potential through modulation of AKT and NF-κB signaling pathways.

Indexed as

AggregatesExtracellular vesiclesHuntington’s diseaseInsulin-like growth factor 2(IGF2)Mutant HuntingtinNuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB)Protein kinase B (AKT)

Identifiers

PMID40713750
PMCPMC12297735

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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.