Evidence map›Paper›PMID 36361836›Full record

ArticleInternational journal of molecular sciences2022

Depletion of Arg1-Positive Microglia/Macrophages Exacerbates Cerebral Ischemic Damage by Facilitating the Inflammatory Response.

Ting Li, Jin Zhao, Hao Gao

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

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

  1. Pooled it
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  11. Detrimental influence of Arginase-1 in infiltrating macrophages on poststroke functional recovery and inflammatory milieu.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  18. Microglia at the blood brain barrier in health and disease.Frontiers in cellular neuroscience · 2024
    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

3 authors at 1 institution in 1 country.

Ting LiGansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.ORCID 0000-0002-6083-1952
Jin ZhaoGansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.
Hao GaoGansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.
Lanzhou University · CN

Funding

National Natural Science Foundation of China 31600831
6 · The paper itself

Abstract

Stroke is a serious worldwide disease that causes death and disability, more than 80% of which is ischemic stroke. The expression of arginase 1 (Arg1), a key player in regulating nitrogen homeostasis, is altered in the peripheral circulation after stroke. Growing evidence indicates that ischemic stroke also induces upregulated Arg1 expression in the central nervous system, especially in activated microglia and macrophages. This implies that Arg1 may affect stroke progression by modulating the cerebral immune response. To investigate the effect of Arg1

Indexed as

Brain InjuriesBrain IschemiaIschemic StrokeStrokeAnimalsArginaseClodronic AcidDisease Models, AnimalIschemiaMacrophagesMiceMice, Inbred C57BLMicrogliaArg1 protein, mouseArginaseClodronic AcidArg1depletioninflammationischemiamicroglia/macrophages

Identifiers

PMID36361836
PMCPMC9655877
OpenAlexW4307423278

What OpenQuestion holds

Textmetadata
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.