Evidence map›Paper›PMID 35093095›Full record

ArticleJournal of translational medicine2022

The ILEI/LIFR complex induces EMT via the Akt and ERK pathways in renal interstitial fibrosis.

Jieqing Zhou, Hong Jiang, Hongkun Jiang, Yan Fan, Jing Zhang, Xiaoxue Ma, Xuewei Yang, Yu Sun, Xing Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 24 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

9 authors at 1 institution in 1 country.

Jieqing ZhouDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Hong JiangDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Hongkun JiangDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Yan FanDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Jing ZhangDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Xiaoxue MaDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Xuewei YangDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Yu SunDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China.
Xing ZhaoDepartment of Pediatrics, First Hospital of China Medical University, Shenyang, 110001, China. zhaoxing_dl@126.com.ORCID 0000-0001-9032-8584
First Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81901658Natural Science Foundation of Liaoning Province 2021-BS-117
6 · The paper itself

Abstract

backgroundChronic kidney disease (CKD) is characterized by high morbidity and mortality and is difficult to cure. Renal interstitial fibrosis (RIF) is a major determinant of, and commonly occurs within, CKD progression. Epithelial mesenchymal transition (EMT) has been identified as a crucial process in triggering renal interstitial fibrosis (RIF). Interleukin-like EMT inducer (ILEI) is an important promotor of EMT; this study aims to elucidate the mechanisms involved.

methodsMale C57BL6/J mouse were randomly divided into 6 groups: sham (n = 10), sham with negative control (NC) shRNA (sham + NC, n = 10), sham with ILEI shRNA (sham + shILEI, n = 10), unilateral ureteral obstruction (UUO, n = 10), UUO with NC (UUO + NC, n = 10) and UUO with ILEI shRNA (UUO + shILEI, n = 10). Hematoxylin and eosin (H&E), Masson, and immunohistochemical (IHC) staining and western blotting (WB) were performed on murine kidney tissue to identify the function and mechanism of ILEI in RIF. In vitro, ILEI was overexpressed to induce EMT in HK2 cells and analyzed via transwell, WB, real-time PCR, and co-immunoprecipitation. Finally, tissue from 12 pediatric CKD patients (seven with RIF and five without RIF) were studied with H&E, Masson, and IHC staining.

resultsOur in vitro model revealed that ILEI facilitates RIF in the UUO model via the Akt and ERK pathways. Further experiments in vivo and in vitro revealed that ILEI promotes renal tubular EMT by binding and activating leukemia inhibitory factor receptor (LIFR), in which phosphorylation of Akt and ERK is involved. We further find markedly increased expression levels of ILEI and LIFR in kidneys from pediatric CKD patients with RIF.

conclusionOur results indicate that ILEI may be a useful biomarker for renal fibrosis and a potential therapeutic target for modulating RIF.

Indexed as

Kidney DiseasesRenal Insufficiency, ChronicAnimalsChildDisease Models, AnimalEpithelial-Mesenchymal TransitionFibrosisHumansLeukemia Inhibitory Factor Receptor alpha SubunitMaleMAP Kinase Signaling SystemMiceProto-Oncogene Proteins c-aktReceptors, OSM-LIFTransforming Growth Factor beta1Leukemia Inhibitory Factor Receptor alpha SubunitLIFR protein, humanProto-Oncogene Proteins c-aktReceptors, OSM-LIFTransforming Growth Factor beta1Epithelial-to-mesenchymal transition (EMT)Interleukin-like epithelial-to-mesenchymal transition inducer (ILEI)Leukemia inhibitory factor receptor (LIFR)Renal interstitial fibrosis (RIF)

Identifiers

PMID35093095
PMCPMC8800269
OpenAlexW4210607638

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.