Evidence map›Paper›PMID 31231213›Full record

ArticleFrontiers in pharmacology2019

Adiponectin Protects Against Cerebral Ischemic Injury Through AdipoR1/AMPK Pathways.

Bin Liu, Jing Liu, Jiangong Wang, Fengjiao Sun, Shujun Jiang, Fengai Hu, Dan Wang, Dunjiang Liu, Cuilan Liu, Haijing Yan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.5field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  15. PGC-1Oxidative medicine and cellular longevity · 2020
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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.

Bin LiuInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Jing LiuInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Jiangong WangInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Fengjiao SunInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Shujun JiangInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Fengai HuInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Dan WangInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Dunjiang LiuInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Cuilan LiuInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Haijing YanInstitute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China.
Binzhou University · CNBinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excitotoxicity induced by excessive N-methyl-D-aspartate (NMDA) receptor activation underlies the pathology of ischemic injury. Adiponectin (APN) is an adipocyte-derived protein hormone that modulates a number of metabolic processes. APN exerts a wide range of biological functions in the central nervous system. However, the role of APN and its receptors in cerebral ischemia/reperfusion (I/R)-induced injury and the related mechanisms remain to be clarified. Here, we found that APN and APN receptor agonist AdipoRon (APR) were protective against excitotoxicity induced by oxygen and glucose deprivation/reperfusion (OGD/R) and NMDA in primary neurons. Adiponectin receptor 1 (AdipoR1) knockdown reversed the protection conferred by either APN or APR. Moreover, the protective effects offered by both APN and APR were compromised by compound C, an inhibitor of amp-activated protein kinase (AMPK) phosphorylation. Both APN and APR protected the dissipation of the ΔΨm caused by OGD/R. They also up-regulated the PGC-1α expression, which was reversed by compound C. Furthermore, both APN and APR ameliorated but APN knockout aggravated the infarct volume and neurological deficient induced by transient middle cerebral artery occlusion (tMCAO)

Indexed as

adiponectinadiponectin receptor 1AdipoRonamp-activated protein kinaseischemiamitochondrialPGC-1α

Identifiers

PMID31231213
PMCPMC6558395
OpenAlexW2945980615

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.