Evidence map›Paper›PMID 39754256›Full record

ReviewCell communication and signaling : CCS2025

Targeting uric acid: a promising intervention against oxidative stress and neuroinflammation in neurodegenerative diseases.

Lin Xu, Chengwei Li, Tiantian Wan, Xinyi Sun, Xiaojie Lin, Dong Yan, Jianjun Li, Penghui Wei

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
–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

38 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. Intrabody B1 targeting TDP-43 modulates neuroinflammatory and metabolic pathways in a preclinical ALS model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  12. Xanthine Oxidase Inhibitory Potential ofInternational journal of molecular sciences · 2026
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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

8 authors.

Lin XuDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Chengwei LiDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Tiantian WanDepartment of Anesthesiology, the First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.
Xinyi SunDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Xiaojie LinDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Dong YanDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Jianjun LiDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China.
Penghui WeiDepartment of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, 758 Hefei Road, Qingdao, China. weipenghuihui@sina.com.

Funding

National Natural Science Foundation of China 82101255Natural Science Foundation of Shandong Province ZR2020MH126Natural Science Foundation of Shandong Province ZR2020QH291Qingdao Key Health Discipline Development Fund QDZDZK2022094Qingdao Outstanding Health Professional Development Fund 2023Scientific Research Foundation of Qilu Hospital of Shandong University QDKY2023QN02
6 · The paper itself

Abstract

Oxidative stress and neuroinflammation are recognized as key factors in the development of neurodegenerative diseases, yet effective interventions and biomarkers to address oxidative stress and neuroinflammation in these conditions are limited. Uric acid (UA), traditionally associated with gout, is now gaining prominence as a potential target in neurodegenerative diseases. Soluble UA stands out as one of the most vital antioxidant compounds produced by the human body, accounting for up to 55% of the extracellular capacity to neutralize free radicals. While there is increasing evidence supporting the neuroprotective properties of UA in Parkinson's disease and Alzheimer's disease, gaps in knowledge still exist regarding the underlying mechanisms and how to effectively translate these benefits into clinical practice. Moreover, the current UA elevation therapy exhibits unstable antioxidant properties, individual variability, and even adverse effects, limiting its potential clinical applications. This review consolidates recent advancements in understanding how UA exerts neuroprotective effects on neurodegenerative diseases and emphasizes the dual roles of UA in managing oxidative stress and neuroinflammation. Additionally, the review elucidates the mechanisms through which UA confers neuroprotection. Based on this, the review underscores the significance of UA as a potential biomarker and aims to provide a comprehensive understanding of its potential as a therapeutic target, while also addressing possible challenges to clinical implementation.

Indexed as

Neurodegenerative DiseasesNeuroinflammatory DiseasesOxidative StressUric AcidAnimalsAntioxidantsBiomarkersHumansNeuroprotective AgentsAntioxidantsBiomarkersNeuroprotective AgentsUric AcidAgeingNeurodegenerative diseasesOxidative stressReactive oxygen speciesUric acid

Identifiers

PMID39754256
PMCPMC11699683

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.