Evidence map›Paper›PMID 35656116›Full record

ArticleAging and disease2022

Blocking C3d

Qi Zhang, Chang Liu, Rubing Shi, Shiyi Zhou, Huimin Shan, Lidong Deng, Tingting Chen, Yiyan Guo, Zhijun Zhang, Guo-Yuan Yang and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

Qi Zhang1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Chang Liu1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Rubing Shi1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Shiyi Zhou1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Huimin Shan1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Lidong Deng1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Tingting Chen1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Yiyan Guo1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Zhijun Zhang1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Guo-Yuan Yang1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Yongting Wang1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Yaohui Tang1School of Biomedical Engineering and Shanghai 6th People's Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes play an essential role in the modulation of blood-brain barrier function. Neurological diseases induce the transformation of astrocytes into a neurotoxic A1 phenotype, exacerbating brain injury. However, the effect of A1 astrocytes on the BBB dysfunction after stroke is unknown. Adult male ICR mice (n=97) were subjected to 90-minute transient middle cerebral artery occlusion (tMCAO). Immunohistochemical staining of A1 (C3d) and A2 (S100A10) was performed to characterize phenotypic changes in astrocytes over time after tMCAO. The glucagon-like peptide-1 receptor agonist semaglutide was intraperitoneally injected into mice to inhibit A1 astrocytes. Infarct volume, atrophy volume, neurobehavioral outcomes, and BBB permeability were evaluated. RNA-seq was adopted to explore the potential targets and signaling pathways of A1 astrocyte-induced BBB dysfunction. Astrocytic C3d expression was increased, while expression of S100A10 was decreased in the first two weeks after tMCAO, reflecting a shift in the astrocytic phenotype. Semaglutide treatment reduced the expression of CD16/32 in microglia and C3d in astrocytes after ischemic stroke (

Indexed as

A1 astrocyteblood-brain barrierischemianeuroinflammationstroke

Identifiers

PMID35656116
PMCPMC9116904
OpenAlexW4282918836

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.