Evidence map›Paper›PMID 32783081›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2020

NLRP6 contributes to inflammation and brain injury following intracerebral haemorrhage by activating autophagy.

Han Xiao, Hui Chen, Rong Jiang, Li Zhang, Lu Wang, Hui Gan, Ning Jiang, Jing Zhao, Xuan Zhai, Ping Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 12% of its field
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

27 citing papers in PubMed, 31 citations in OpenAlex.

  1. Lipid metabolism, microglia, and stroke.Neural regeneration research · 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

10 authors at 2 institutions in 1 country.

Han XiaoDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Hui ChenDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Rong JiangLaboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing, China.
Li ZhangDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Lu WangDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Hui GanDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Ning JiangInstitute of Neuroscience, Chongqing Medical University, Chongqing, China.
Jing ZhaoInstitute of Neuroscience, Chongqing Medical University, Chongqing, China.
Xuan ZhaiDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Ping LiangDepartment of Neurosurgery, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China. liangping868@sina.com.ORCID 0000-0002-7409-9504
China International Science and Technology Cooperation · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a crucial factor contributing to secondary brain injury after intracerebral haemorrhage (ICH). NLRP6, a member of nod-like receptors (NLRs) family, has been reported to participate in inflammation and host-defence in multiple diseases. Distinct from the other NLR family members, NLRP6 regulates inflammation in an inflammasome-dependent as well as an inflammasome-independent pathway. However, the role of NLRP6 in regulating signalling pathways during ICH is poorly understood. In the present study, we demonstrated that NLRP6 expression was upregulated after ICH, both in humans and in rats. Subsequently, we developed a rat model of ICH and found that NLRP6 knockdown reduced brain injury, alleviated inflammation, and suppressed autophagy following ICH. Further, results indicated that autophagy involved in NLRP6 mediated inflammation after ICH. Moreover, we found that NLRP6 mediated regulation of autophagy and inflammation was inflammasome-dependent. This study revealed the underlying molecular mechanism of NLRP6 in inflammation and highlights the therapeutic potential of targeting NLRP6 in secondary brain injury after ICH. KEY MESSAGES: • NLRP6 was upregulated following ICH in humans and rats. • NLRP6 knockdown reduced brain injury, alleviated inflammation, and suppressed autophagy following ICH. • NLRP6 aggravated inflammation after ICH by activating autophagy. • NLRP6 regulated inflammation and autophagy after ICH by activating inflammasome pathway.

Indexed as

AutophagyAnimalsBiomarkersBrain InjuriesCerebral HemorrhageDisease Models, AnimalDisease SusceptibilityGene ExpressionHumansImmunohistochemistryInflammasomesInflammationRatsReceptors, AngiotensinReceptors, VasopressinSignal TransductionBiomarkersInflammasomesNlrp6 protein, ratReceptors, AngiotensinReceptors, VasopressinAutophagyInflammasomeInflammationIntracerebral haemorrhageNLRP6

Identifiers

PMID32783081
OpenAlexW3048569556

What OpenQuestion holds

Textmetadata
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.