Evidence map›Paper›PMID 42469634›Full record

ArticleMolecular medicine (Cambridge, Mass.)2026

Secretory leukocyte protease inhibitor (SLPI) attenuates TLR4/NF-κB-mediated neuroinflammation in amyotrophic lateral sclerosis: a candidate molecule associated with neuro-pathology.

Ming-An Li, Yi-Zhi Song, Ting Li, Jian Wu, Yue Tao, Rui Hu, Chen-Meng Qiao, Chun Cui, Wei-Jiang Zhao, Yan-Qin Shen

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Ming-An LiLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Yi-Zhi SongLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Ting LiLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Jian WuLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Yue TaoLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Rui HuLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Chen-Meng QiaoLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Chun CuiLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China.
Wei-Jiang ZhaoLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China. weijiangzhao@jiangnan.edu.cn.ORCID http://orcid.org/0000-0002-6556-2827
Yan-Qin ShenLaboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, 1800 Lihu Avenue, Binhu District, Wuxi, Jiangsu, 214122, China. shenyanqin@jiangnan.edu.cn.ORCID http://orcid.org/0000-0003-1724-4135

Funding

National Natural Science Foundation of China 82171429Postgraduate Research & Practice Innovation Program of Jiangsu Province KYCX25_2743
6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disorder driven by neuroinflammation involving activated microglia and astrocytes, which accelerates the loss of motor neurons. While Secretory leukocyte protease inhibitor (SLPI) is known for its immunomodulatory properties, its specific role in ALS pathogenesis has not been fully established. This study aimed to characterize the expression patterns and functional significance of SLPI in ALS models.

methodsThe study utilized SOD1

resultsIn SOD1

conclusionsThe dynamic changes in SLPI levels suggest its potential relevance as a candidate molecule for disease staging. Meanwhile, its protective effects in regulating inflammation suggest that it could be a promising therapeutic candidate for mitigating ALS-associated neuroinflammation.

Indexed as

Amyotrophic Lateral SclerosisNeuroinflammatory DiseasesNF-kappa BSecretory Leukocyte Peptidase InhibitorToll-Like Receptor 4AnimalsAstrocytesCell LineDisease Models, AnimalHumansInflammationMaleMiceMice, TransgenicMicrogliaMotor NeuronsNF-kappa BSecretory Leukocyte Peptidase InhibitorToll-Like Receptor 4ALSAstrocyteMicrogliaMotor neuronsNeuroinflammationOxidative StressSLPISOD1G93A mice

Identifiers

PMID42469634
PMCPMC13660176

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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.