Evidence map›Paper›PMID 40789938›Full record

ArticleActa pharmacologica Sinica2026

NADPH acts as an endogenous P2X7 receptor modulator to gate neuroinflammatory responses of microglia.

Yu-Jie Mou, Feng-Min Li, Jun-Tong Lou, Hai-Yue Tu, Yi Zhu, Rui Sheng, Zhong-Ling Zhang, Yu-Zheng Zhao, Fu-Hai Ji, Jun-Chao Wu and 1 more

Abstract read
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In one paragraph

Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026
    Review
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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

11 authors.

Yu-Jie Mou *Department of Anesthesiology, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Feng-Min Li *Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.
Jun-Tong LouDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.
Hai-Yue TuInstitutes for Translational Medicine, Suzhou Medical College of Soochow University, Suzhou, 215123, China.
Yi ZhuDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.
Rui ShengDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.
Zhong-Ling ZhangDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Yu-Zheng ZhaoOptogenetics & Synthetic Biology Interdisciplinary Research Center, State Key Laboratory of Bioreactor Engineering, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, 200237, China.
Fu-Hai JiDepartment of Anesthesiology, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Jun-Chao WuDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China. wujunchao@suda.edu.cn.
Zheng-Hong QinDepartment of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China. qinzhenhong@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced nicotinamide adenine dinucleotide phosphate (NADPH) is an important coenzyme involved in cellular biosynthetic and redox metabolism. It has been recognized for its role in regulating neuroinflammation through coordinating redox reactions. Whether there are new actions other than redox regulation remain unclear. In this study we investigated a novel mechanism by which NADPH regulated microglia-mediated neuroinflammation. We showed that NADPH application significantly alleviated NLRP3 inflammasome activation in microglia and exerted neuroprotective effects both in vitro and in vivo neuroinflammation models. With P2X7R knockdown microglial cells and P2X7R

Indexed as

MicrogliaNADPNeuroinflammatory DiseasesReceptors, Purinergic P2X7Adenosine TriphosphateAnimalsCell LineInflammasomesMaleMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinPurinergic P2X Receptor AntagonistsPyridinesTetrazoles3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridineAdenosine TriphosphateInflammasomesNADPNLR Family, Pyrin Domain-Containing 3 ProteinP2rx7 protein, mousePurinergic P2X Receptor AntagonistsPyridinesReceptors, Purinergic P2X7TetrazolesmicrogliaNADPHneuroinflammation.NLRP3 inflammationP2X7 receptor

Identifiers

PMID40789938
PMCPMC12764979

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Registered trials

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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.