Evidence map›Paper›PMID 38196698›Full record

ArticleTranslational andrology and urology2023

Klotho activation of Nrf2 inhibits the ferroptosis signaling pathway to ameliorate sepsis-associated acute kidney injury.

Pan Zhou, Congcong Zhao, Yuhong Chen, Xuefang Liu, Chunxue Wu, Zhenjie Hu

Open access · diamondAbstract read
In one paragraph

Article in Translational andrology and urology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-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

17 citing papers in PubMed, 18 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

6 authors at 4 institutions in 1 country.

Pan ZhouDepartment of Critical Care Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Congcong ZhaoDepartment of Critical Care Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Yuhong ChenDepartment of Critical Care Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Xuefang LiuDepartment of Anesthesiology and Intensive Care Unit, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Chunxue WuIntensive Care Unit of Emergency Department, Neurology Branch of Cangzhou Central Hospital, Cangzhou, China.
Zhenjie HuDepartment of Critical Care Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Hebei Medical University · CNCangzhou Central Hospital · CNFourth Hospital of Hebei Medical University · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Sepsis-associated acute kidney injury (SA-AKI) is a common complication of sepsis and greatly increases patient mortality. Recombinant human Klotho protein (Klotho) is a protective protein that can be secreted by the kidney. The aim of this study was to explore the protective effect of Klotho on SA-AKI and its molecular mechanism. Methods: Results: Klotho reduced the release of renal injury markers and inflammatory cytokines, decreased oxidative stress, improved renal histopathological changes, ameliorated mitochondrial damage in mouse renal tubular epithelial cells, increased HK2 cell viability and reduced reactive oxygen species (ROS) accumulation. Exogenous supplementation with Klotho increased the Klotho content in circulating blood, renal tissue and HK2 cells. Conclusions: In the SA-AKI model, Klotho attenuated renal tissue injury, increased HK2 cell viability, decreased inflammatory factor expression and oxidative stress, restored tubular epithelial mitochondrial function, and increased its level in circulating blood, renal tissue and HK2 cells. Klotho probably exerts its protective effects by activating Nrf2 to inhibit the ferroptosis signaling pathway.

Indexed as

ferroptosisKlothooxidative stressSepsis-associated acute kidney injury (SA-AKI)

Identifiers

PMID38196698
PMCPMC10772648
OpenAlexW4390233685

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.