Evidence map›Paper›PMID 31043581›Full record

ArticleCell death & disease2019

ALK5 signaling pathway mediates neurogenesis and functional recovery after cerebral ischemia/reperfusion in rats via Gadd45b.

Keming Zhang, Qinbin Zhang, Jing Deng, Jinfang Li, Jiani Li, Lan Wen, Jingxi Ma, Changqing Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 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 3 institutions in 1 country.

Keming ZhangDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qinbin ZhangDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID http://orcid.org/0000-0002-9772-1511
Jing DengDepartment of Neurology, Chongqing General Hospital, Chongqing, China.
Jinfang LiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jiani LiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Lan WenDepartment of Neurology, The Southwest Hospital, Chongqing, China.
Jingxi MaDepartment of Neurology, Chongqing General Hospital, Chongqing, China.
Changqing LiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. Licq@hospital.cqmu.edu.cn.
Dalian Medical University · CNFirst People's Hospital of Chongqing · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor β (TGF-β) serves critical functions in brain injury, especially in cerebral ischemia; however, apart from its neuroprotective effects, its role in regulating neurogenesis is unclear. TGF-β acts in different ways; the most important, canonical TGF-β activity involves TGF-β receptor I (TβRI) or the activin receptor-like kinase 5 (ALK5) signaling pathway. ALK5 signaling is a major determinant of adult neurogenesis. In our previous studies, growth arrest and DNA damage protein 45b (Gadd45b) mediated axonal plasticity after stroke. Here, we hypothesized that ALK5 signaling regulates neural plasticity and neurological function recovery after cerebral ischemia/reperfusion (I/R) via Gadd45b. First, ALK5 expression was significantly increased in middle cerebral artery occlusion/reperfusion (MCAO/R) rats. Then, we knocked down or overexpressed ALK5 with lentivirus (LV) in vivo. ALK5 knockdown reduced axonal and dendritic plasticity, with a concomitant decrease in neurological function recovery. Conversely, ALK5 overexpression significantly increased neurogenesis as well as functional recovery. Furthermore, ALK5 mediated Gadd45b protein levels by regulating Smad2/3 phosphorylation. Finally, ALK5 coimmunoprecipitated with Gadd45b. Our results suggested that the ALK5 signaling pathway plays a critical role in mediating neural plasticity and neurological function recovery via Gadd45b after cerebral ischemia, representing a new potential target for cerebral I/R injury.

Indexed as

AnimalsAntigens, DifferentiationBrainCerebrovascular DisordersDisease Models, AnimalGADD45 ProteinsGene Expression RegulationMaleMiddle Cerebral ArteryNeurogenesisNeuronal PlasticityNeuronsPhosphorylationRatsRats, Sprague-DawleyReceptor, Transforming Growth Factor-beta Type IAntigens, DifferentiationGadd45b protein, ratGADD45 ProteinsReceptor, Transforming Growth Factor-beta Type IRNA, Small InterferingSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad3 protein, ratTgfbr1 protein, ratTransforming Growth Factor beta

Identifiers

PMID31043581
PMCPMC6494915
OpenAlexW2943546666

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.