Evidence map›Paper›PMID 42615346›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease.

Luyao Li, Hao Tang, Qin Yu, Yuyang Zhang, Binglu Shi, Ying Kong, Leiyu Xu, Jingjing Shao, Chenghong Hu, Lingyu She and 6 more

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

16 authors.

Luyao LiZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.ORCID https://orcid.org/0000-0001-9457-8329
Hao TangZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Qin YuZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Yuyang ZhangZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Binglu ShiZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Ying KongZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Leiyu XuZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Jingjing ShaoZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Chenghong HuZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Lingyu SheSchool of Pharmacy, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Zhe WangZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Haiyi ChenZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Aleksandr V SamorodovDepartment of Pharmacology, Bashkir State Medical University, Ufa, Russia.
Gang CaoSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Xia ZhaoSchool of Pharmacy, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Yi WangZhejiang Provincial Key Laboratory of Anti-Cancer Chinese Medicines and Natural Medicines, School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China.ORCID https://orcid.org/0009-0005-9347-4946

Funding

Innovation Team of Hangzhou City TD2024002Interdisciplinary Research Project of Hangzhou Normal University 2024JCXK06National Natural Science Foundation of China 82361138563National Natural Science Foundation of China 82501725
6 · The paper itself

Abstract

Neuroinflammation driven by microglial activation is a defining feature of Alzheimer's disease (AD), yet the molecular mechanisms sustaining this proinflammatory state remain unclear. Here, we identify the deubiquitinase OTUD7B as a critical regulator of microglial activation and AD pathology. OTUD7B expression was markedly elevated in microglia from AD mouse models and human patient datasets. Genetic ablation of OTUD7B markedly attenuated microglial activation and cytokine release, alleviated neuronal injury, and improved cognitive performance in AD mice. Mechanistically, OTUD7B directly interacted with STAT3 and removed K48-linked ubiquitin chains at lysine 283, thereby stabilizing STAT3, promoting its nuclear translocation, and enhancing transcription of proinflammatory mediators. Integrative transcriptomic analysis revealed that OTUD7B deficiency suppressed proinflammatory transcriptional programs in microglia. Together, these findings uncover an OTUD7B-STAT3 signaling axis that sustains microglial-driven neuroinflammation and identify OTUD7B as a potential therapeutic target for mitigating neurodegenerative pathology in AD.

Indexed as

alzheimer's diseasedeubiquitinating enzymesmicroglialneuroinflammationOTUD7BSTAT3

Identifiers

PMID42615346
PMCPMC13487723

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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.