Evidence map›Paper›PMID 39635882›Full record

ArticleAutophagy2025

Upregulation of ISG15 induced by MAPT/tau accumulation represses autophagic flux by inhibiting HDAC6 activity: a vicious cycle in Alzheimer disease.

Qian Liu, Xin Wang, Zhi-Ting Fang, Jun-Ning Zhao, Xue-Xiang Rui, Bing-Ge Zhang, Ye He, Rui-Juan Liu, Jian Chen, Gao-Shang Chai and 1 more

Abstract read
In one paragraph

Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. When ISG15 is involved in inflammation.Frontiers in immunology · 2026
    Review
  7. Review
  8. Cholestanol promotes tau pathology in a mouse model of tauopathy.Cellular and molecular life sciences : CMLS · 2025
    Article
  9. Article
  10. Article
  11. 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.

Qian LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0002-7849-9871
Xin WangDepartment of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-7440-3150
Zhi-Ting FangDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0000-1606-041X
Jun-Ning ZhaoDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0009-1068-5377
Xue-Xiang RuiDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0009-4011-142X
Bing-Ge ZhangDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0008-7528-3101
Ye HeDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0007-7130-6241
Rui-Juan LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0006-6461-9912
Jian ChenDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0000-6503-3805
Gao-Shang ChaiMOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Department of Fundamental Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China.ORCID 0000-0002-1943-3717
Gong-Ping LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-8501-998X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer disease (AD), a prevalent neurodegenerative condition in the elderly, is marked by a deficit in macroautophagy/autophagy, leading to intracellular MAPT/tau accumulation. While ISG15 (ISG15 ubiquitin like modifier) has been identified as a regulator of selective autophagy in ataxia telangiectasia (A-T), its role in AD remains unexplored. Our study reveals elevated ISG15 levels in the brains of patients with sporadic AD and AD models

Indexed as

Alzheimer DiseaseAutophagyCytokinesHistone Deacetylase 6tau ProteinsUbiquitinsUp-RegulationAgedAnimalsAutophagosomesBrainHEK293 CellsHumansLysosomesMaleMiceCytokinesHDAC6 protein, humanHistone Deacetylase 6ISG15 protein, humanMAPT protein, humantau ProteinsUbiquitinsAlzheimer diseaseautophagycognitionISG15MAPT

Identifiers

PMID39635882
PMCPMC11925114

What OpenQuestion 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 OpenQuestion graph.