Evidence map›Paper›PMID 33643819›Full record

ArticleActa pharmaceutica Sinica. B2021

Gene deficiency or pharmacological inhibition of PDCD4-mediated FGR signaling protects against acute kidney injury.

Xu Jing, Dandan Ren, Fei Gao, Ye Chen, Xiao Wu, Yue Han, Qingsheng Han, Liang Li, Xiaojie Wang, Wei Tang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 28 citations in OpenAlex.

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  8. Targeting RNA oxidation by ISG20-mediated degradation is a potential therapeutic strategy for acute kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
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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

11 authors at 2 institutions in 1 country.

Xu JingDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Dandan RenDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Fei GaoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.
Ye ChenDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Xiao WuThe Key Laboratory of Cardiovascular Remodeling and Function Research, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.
Yue HanDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Qingsheng HanDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Liang LiDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Xiaojie WangDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Wei TangDepartment of Microbiology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Yan ZhangDepartment of Pharmacology, School of Basic Medical Science, Shandong University, Jinan 250012, China.
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that programmed cell death 4 (PDCD4) modulates distinct signal transduction pathways in different pathological conditions. Despite acute and chronic immune responses elicited by ischemia contributing to the functional deterioration of the kidney, the contributions and mechanisms of PDCD4 in acute kidney injury (AKI) have remained unclear. Using two murine AKI models including renal ischemia/reperfusion injury (IRI) and cisplatin-induced AKI, we found that PDCD4 deficiency markedly ameliorated renal dysfunction and inflammatory responses in AKI mice. Consistently, upregulation of PDCD4 was also confirmed in the kidneys from patients with biopsy confirmed acute tubular necrosis from a retrospective cohort study. Moreover, we found that overexpression of

Indexed as

Acute kidney injuryCell deathFGRInflammationIschemia–reperfusion injuryNOTCH1PDCD4Tyrosine kinase

Identifiers

PMID33643819
PMCPMC7893143
OpenAlexW3095927968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.