Evidence map›Paper›PMID 35596061›Full record

ArticleExperimental & molecular medicine2022

Loss of RTN3 phenocopies chronic kidney disease and results in activation of the IGF2-JAK2 pathway in proximal tubular epithelial cells.

Liang-Liang Fan, Ran Du, Ji-Shi Liu, Jie-Yuan Jin, Chen-Yu Wang, Yi Dong, Wan-Xia He, Ri-Qiang Yan, Rong Xiang

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 13 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 2 institutions in 2 countries.

Liang-Liang Fan *Department of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Ran Du *Department of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Ji-Shi Liu *Department of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Jie-Yuan JinDepartment of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Chen-Yu WangDepartment of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Yi DongDepartment of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Wan-Xia HeDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, 06032, United States.
Ri-Qiang YanDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, 06032, United States. riyan@uchc.edu.
Rong XiangDepartment of Nephrology, Third Xiangya Hospital of Central South University, Changsha, 410013, China. shirlesmile@csu.edu.cn.ORCID http://orcid.org/0000-0002-5521-3615
Central South University · CNUConn Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reticulon 3 (RTN3) is an endoplasmic reticulum protein that has previously been shown to play roles in neurodegenerative diseases, but little is known about its function in the kidneys. The aim of the present study was to clarify the roles of RTN3 in chronic kidney disease (CKD) and kidney fibrosis. In this study, RTN3 levels were measured in kidney tissues from healthy controls and CKD or kidney fibrosis patients. An RTN3-null mouse model was generated to explore the pathophysiological roles of RTN3 in the kidneys. The underlying mechanisms were studied in primary proximal tubular epithelial cells and HEK293 cells in vitro. The results showed that (1) a reduction in RTN3 in mice induces CKD and kidney fibrosis; (2) decreased RTN3 expression is found in patients with CKD; (3) RTN3 plays critical roles in regulating collagen biosynthesis and mitochondrial function; and (4) mechanistically, RTN3 regulates these phenotypes by interacting with GC-Rich Promoter Binding Protein 1 (GPBP1), which activates the IGF2-JAK2-STAT3 pathway. Our study indicates that RTN3 might play crucial roles in CKD and kidney fibrosis and that a reduction in RTN3 in the kidneys might be a risk factor for CKD and kidney fibrosis.

Indexed as

Membrane ProteinsNerve Tissue ProteinsRenal Insufficiency, ChronicAnimalsBlood ProteinsCarrier ProteinsDNA-Binding ProteinsEpithelial CellsFibrosisHEK293 CellsHumansInsulin-Like Growth Factor IIJanus Kinase 2KidneyMicePhenotypeBlood ProteinsCarrier ProteinsDNA-Binding ProteinsGPBP1 protein, humanIGF2 protein, humanInsulin-Like Growth Factor IIJAK2 protein, humanJanus Kinase 2Membrane ProteinsNerve Tissue ProteinsRTN3 protein, human

Identifiers

PMID35596061
PMCPMC9166791
OpenAlexW4280490236

What OpenQuestion holds

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LicenceCC BY
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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.