Evidence map›Paper›PMID 35148669›Full record

ArticleBioengineered2022

Circular RNA HIPK3 aggravates sepsis-induced acute kidney injury via modulating the microRNA-338/forkhead box A1 axis.

Hulin Lu, Yan Chen, Xiaoyi Wang, Yong Yang, Min Ding, Fengping Qiu

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. HNF3α Targets Nckap1l and Promotes Renal Fibrosis Following Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  6. Article
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  13. Article
  14. Circular RNAs in organ injury: recent development.Journal of translational medicine · 2022
    Review
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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 1 institution in 1 country.

Hulin LuDepartment of Nephrology, Huzhou First People's Hospital, Huzhou, China.
Yan ChenDepartment of Infectious Disease, Huzhou First People's Hospital, Huzhou, China.ORCID 0000-0002-2432-825X
Xiaoyi WangDepartment of Nephrology, Huzhou First People's Hospital, Huzhou, China.
Yong YangDepartment of Nephrology, Huzhou First People's Hospital, Huzhou, China.
Min DingDepartment of Nephrology, Huzhou First People's Hospital, Huzhou, China.
Fengping QiuDepartment of Nephrology, Huzhou First People's Hospital, Huzhou, China.
Third People's Hospital of Huzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular RNAs (circRNAs) have been extensively studied in various diseases, including sepsis-induced acute kidney injury (AKI). This research intended to elucidate the mechanism of circular RNA HIPK3 (circHIPK3) in sepsis-engendered AKI. Human tubule epithelial cells (HK2) were stimulated with lipopolysaccharide (LPS) to establish a septic AKI cell model. The gene expression levels were evaluated by RT-qPCR. Cell viability, apoptosis, and cell cycle distribution were assessed through CCK-8 and flow cytometry assays. The potential interactions between genes were verified by luciferase reporter and RIP assays. The results displayed that circHIPK3 expression was enhanced in septic AKI patients and LPS-triggered HK2 cells. Moreover, circHIPK3 interference expedited HK2 cell viability and attenuated apoptosis, inflammatory and oxidative damages following LPS stimulation. Furthermore, circHIPK3 functioned as a molecular sponge for miR-338, and forkhead box A1 (FOXA1) was negatively regulated by miR-338. CircHIPK3 aggravated cell injury in LPS-treated HK2 via targeting miR-338, and FOXA1 addition overturned the suppressing impacts of miR-338-3p augmentation on LPS-activated HK2 cell damage. Finally, we demonstrated that circHIPK3 modulated LPS-induced cell damage via the miR-338/FOXA1 axis. In sum, our results elaborated that circHIPK3 knockdown attenuated LPS-triggered HK2 cell injury by regulating FOXA1 expression via interacting with miR-338, suggesting that circHIPK3 might be a potential biomarker and therapeutic target for sepsis-induced AKI patients.

Indexed as

Acute Kidney InjuryMicroRNAsSepsisApoptosisHepatocyte Nuclear Factor 3-alphaHumansIntracellular Signaling Peptides and ProteinsLipopolysaccharidesProtein Serine-Threonine KinasesRNA, CircularFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaHIPK3 protein, humanIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMicroRNAsMIRN338 microRNA, humanProtein Serine-Threonine KinasesRNA, Circularacute kidney injuryCircHIPK3FOXA1miR-338Sepsis

Identifiers

PMID35148669
PMCPMC8974176
OpenAlexW4211116799

What Socratic 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 Socratic graph.