Evidence map›Paper›PMID 38565402›Full record

ArticleJournal of advanced research2025

Exercise-Induced Reduction of IGF1R Sumoylation Attenuates Neuroinflammation in APP/PS1 Transgenic Mice.

Yisheng Chen, Xiaofeng Chen, Zhiwen Luo, Xueran Kang, Yunshen Ge, Renwen Wan, Qian Wang, Zhihua Han, Fangqi Li, Zhongcheng Fan and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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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

19 authors at 10 institutions in 2 countries.

Yisheng ChenHuashan Hospital, Fudan University, Shanghai, China.
Xiaofeng ChenDepartment of Orthopaedics, National Regional Medical Center, Jinjiang Municipal Hospital,Shanghai Sixth People's Hospital, Fujian, Jinjiang,China. Electronic address: feng5313@hotmail.com.
Zhiwen LuoHuashan Hospital, Fudan University, Shanghai, China.
Xueran KangShanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, China.
Yunshen GeHuashan Hospital, Fudan University, Shanghai, China.
Renwen WanHuashan Hospital, Fudan University, Shanghai, China.
Qian WangDepartment of Central Laboratory, The Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China.
Zhihua HanDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai 200080, China.
Fangqi LiHuashan Hospital, Fudan University, Shanghai, China.
Zhongcheng FanDepartment of Orthopaedic Surgery, Hainan Province Clinical Medical Center, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, China.
Yuchun XieJiangsu Province Geriatric Hospital, China.
Beijie QiHuashan Hospital, Fudan University, Shanghai, China.
Xintao ZhangDepartment of Sports Medicine and Rehabilitation, Peking University Shenzhen Hospital Lianhua Road, Shenzhen City, Guangdong Province, China.
Zhenwei YangDepartment of Orthopaedics, First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, China.
John H ZhangDepartment of Neurosurgery, Department of Physiology and Pharmacology, Department of Neurosurgery and Anesthesiology, School of Medicine, Loma Linda University, Risley Hall, Room 219, 11041 Campus Street, Loma Linda, CA, 92354, USA. Electronic address: johnzhang3910@yahoo.com.
Danping LiuDepartment of Orthopaedics, First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, China. Electronic address: liudanping2009@sohu.com.
Yuzhen XuDepartment of Rehabilitation, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, China. Electronic address: tianyayizhe@126.com.
Dongyan WuHuashan Hospital, Fudan University, Shanghai, China. Electronic address: walkwinter@163.com.
Shiyi ChenHuashan Hospital, Fudan University, Shanghai, China. Electronic address: cshiyi@163.com.
Fudan University · CNJinzhou Medical University · CNShanghai Jiao Tong University · CNAffiliated Hospital of Taishan Medical University · CNCentral South University · CNJiangsu Province Hospital · CNLoma Linda University · USPeking University Shenzhen Hospital · CNQingdao University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlzheimer's Disease (AD), a progressive neurodegenerative disorder, is marked by cognitive deterioration and heightened neuroinflammation. The influence of Insulin-like Growth Factor 1 Receptor (IGF1R) and its post-translational modifications, especially sumoylation, is crucial in understanding the progression of AD and exploring novel therapeutic avenues.

objectivesThis study investigates the impact of exercise on the sumoylation of IGF1R and its role in ameliorating AD symptoms in APP/PS1 mice, with a specific focus on neuroinflammation and innovative therapeutic strategies.

methodsAPP/PS1 mice were subjected to a regimen of moderate-intensity exercise. The investigation encompassed assessments of cognitive functions, alterations in hippocampal protein expressions, neuroinflammatory markers, and the effects of exercise on IGF1R and SUMO1 nuclear translocation. Additionally, the study evaluated the efficacy of KPT-330, a nuclear export inhibitor, as an alternative to exercise.

resultsExercise notably enhanced cognitive functions in AD mice, possibly through modulations in hippocampal proteins, including Bcl-2 and BACE1. A decrease in neuroinflammatory markers such as IL-1β, IL-6, and TNF-α was observed, indicative of reduced neuroinflammation. Exercise modulated the nuclear translocation of SUMO1 and IGF1R in the hippocampus, thereby facilitating neuronal regeneration. Mutant IGF1R (MT IGF1R), lacking SUMO1 modification sites, showed reduced SUMOylation, leading to diminished expression of pro-inflammatory cytokines and apoptosis. KPT-330 impeded the formation of the IGF1R/RanBP2/SUMO1 complex, thereby limiting IGF1R nuclear translocation, inflammation, and neuronal apoptosis, while enhancing cognitive functions and neuron proliferation.

conclusionModerate-intensity exercise effectively mitigates AD symptoms in mice, primarily by diminishing neuroinflammation, through the reduction of IGF1R Sumoylation. KPT-330, as a potential alternative to physical exercise, enhances the neuroprotective role of IGF1R by inhibiting SUMOylation through targeting XPO1, presenting a promising therapeutic strategy for AD.

Indexed as

Alzheimer DiseaseNeuroinflammatory DiseasesNeuroprotectionPhysical Conditioning, AnimalReceptor, IGF Type 1AnimalsApoptosisDisease Models, AnimalHydrazinesMaleMiceMice, Inbred C57BLMice, TransgenicMolecular ChaperonesMorris Water Maze TestNeuroprotective AgentsHydrazinesIgf1r protein, mouseMolecular ChaperonesNeuroprotective AgentsNuclear Pore Complex Proteinsran-binding protein 2Receptor, IGF Type 1selinexorSUMO-1 ProteinSumo1 protein, mouseTriazolesAlzheimer's DiseaseExerciseIGF1R sumoylationKPT-330NeuroinflammationSUMOylation inhibitor

Identifiers

PMID38565402
PMCPMC11954827
OpenAlexW4393359215

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.