Evidence map›Paper›PMID 32703968›Full record

ArticleCell death & disease2020

Catalytically inactive RIP1 and RIP3 deficiency protect against acute ischemic stroke by inhibiting necroptosis and neuroinflammation.

Yue Zhang, Ming Li, Xiaoming Li, Haiwei Zhang, Lingxia Wang, Xiaoxia Wu, Haibing Zhang, Yan Luo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Yue ZhangDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.ORCID http://orcid.org/0000-0002-7727-4814
Ming LiCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China.
Xiaoming LiCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China.
Haiwei ZhangCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China.
Lingxia WangCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China.
Xiaoxia WuCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China.
Haibing ZhangCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 200031, Shanghai, China. hbzhang@sibs.ac.cn.
Yan LuoDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. ly11087@rjh.com.cn.
Shanghai Institute of Nutrition and Health · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis, which is mediated by RIP1/RIP3/MLKL (receptor-interacting protein kinase 1/receptor-interacting protein kinase 3/mixed lineage kinase domain-like protein) signaling, is a critical process in the development of acute ischemic stroke. However, it is unclear precisely how necroptosis promotes the pathogenesis of acute ischemic stroke. In this experimental study in mice, we investigated how necroptosis loss-of-function mice, RIP1 kinase-dead mice, RIP3-deficiency mice, and MLKL-deficiency mice could be protected against cerebral injury after acute ischemic stroke. Insoluble RIP1, RIP3, and MLKL were all detected in the infarct area of the study mice, indicating activation of necroptosis. Two types of RIP1 kinase-dead mutant mice (Rip1

Indexed as

NecroptosisAcute DiseaseAnimalsBiocatalysisBrainCell DeathInfarction, Middle Cerebral ArteryInflammationIschemic StrokeMice, Inbred C57BLMutationNF-kappa BProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionMLKL protein, mouseNF-kappa BProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouseRipk3 protein, mouse

Identifiers

PMID32703968
PMCPMC7378260
OpenAlexW3044760548

What OpenQuestion holds

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LicenceCC BY
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.