Evidence map›Paper›PMID 30314894›Full record

ArticleEBioMedicine2018

Endoplasmic reticulum stress is activated in post-ischemic kidneys to promote chronic kidney disease.

Shaoqun Shu, Jiefu Zhu, Zhiwen Liu, Chengyuan Tang, Juan Cai, Zheng Dong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 146 citations in OpenAlex.

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  20. Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024
    Review

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Shaoqun ShuDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.
Jiefu ZhuDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, GA, USA.
Zhiwen LiuDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.
Chengyuan TangDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.
Juan CaiDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.
Zheng DongDepartment of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, GA, USA. Electronic address: zdong@csu.edu.cn.
Second Xiangya Hospital of Central South University · CNCentral South University · CNCharlie Norwood VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) may lead to the development of chronic kidney disease (CKD), i.e. AKI-CKD transition, but the underlying mechanism remains largely unclear. Endoplasmic reticulum (ER) stress is characterized by the accumulation of unfolded or misfolded proteins in ER resulting in a cellular stress response. The role of ER stress in AKI-CKD transition remains unknown.

methodsIn this study, we examined ER stress in the mouse model of AKI-CKD transition after unilateral renal ischemia-reperfusion injury (uIR). To determine the role of ER stress in AKI-CKD transition, we tested the effects of two chemical chaperones: Tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid (4-PBA).

findingsuIR led to the induction of ER stress in kidneys, as indicated by increased expression of UPR molecules CHOP (C/EBP homologous protein) and BiP(binding immunoglobulin protein; also called GRP78-78 kDa glucose-regulated protein). Given at 3 days after uIR, both TUDCA and 4-PBA blocked ER stress in post-ischemic kidneys. Notably, both chemicals promoted renal recovery and suppressed tubulointerstitial injury as manifested by the reduction of tubular atrophy, renal fibrosis and myofibroblast activation. Inhibition of ER stress further attenuated renal tubular epithelial cell apoptosis, inflammation and autophagy in post-ischemic kidneys.

interpretationThese findings suggest that ER stress contributes critically to the development of chronic kidney pathologies and CKD following AKI, and inhibition of ER stress may represent a potential therapeutic strategy to impede AKI-CKD transition.

Indexed as

Acute Kidney InjuryEndoplasmic Reticulum StressRenal Insufficiency, ChronicReperfusion InjuryAnimalsDisease Models, AnimalEndoplasmic Reticulum Chaperone BiPMaleMiceEndoplasmic Reticulum Chaperone BiPAKI-CKD transitionApoptosisAutophagyER stressFibrosisRenal ischemia-reperfusion

Identifiers

PMID30314894
PMCPMC6286638
OpenAlexW2897975801

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.