Evidence map›Paper›PMID 29497029›Full record

ArticleCell death & disease2018

Ischemic preconditioning attenuates ischemia/reperfusion-induced kidney injury by activating autophagy via the SGK1 signaling pathway.

Ying Xie, Daofang Jiang, Jing Xiao, Chensheng Fu, Zhenxing Zhang, Zhibin Ye, Xiaoli Zhang

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 76 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

7 authors at 2 institutions in 1 country.

Ying XieDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.
Daofang JiangDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-2461-419X
Jing XiaoDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.
Chensheng FuDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.
Zhenxing ZhangDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.
Zhibin YeDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China.
Xiaoli ZhangDepartment of Nephrology, Huadong Hospital, Fudan University, Shanghai, China. drzhxl@163.com.
Fudan University · CNHuadong Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic preconditioning (IPC) has a strong renoprotective effect during renal ischemia/reperfusion (I/R) injury that is thought to relate to autophagy. However, the role of autophagy during IPC-afforded renoprotection and the precise mechanisms involved are unknown. In this study, an in vitro hypoxia/reoxygenation (H/R) model was established in which oxygen and glucose deprivation (OGD) was applied to renal cells for 15 h followed by reoxygenation under normal conditions for 30 min, 2 h or 6 h; transient OGD and subsequent reoxygenation were implemented before prolonged H/R injury to achieve hypoxic preconditioning (HPC). 3-Methyladenine (3-MA) was used to inhibit autophagy. In a renal I/R injury model, rats were subjected to 40 min of renal ischemia followed by 6 h, 12 h or 24 h of reperfusion. IPC was produced by four cycles of ischemia (8 min each) followed by 5 min of reperfusion prior to sustained ischemia. We found that IPC increased LC3II and Beclin-1 levels and decreased SQSTM/p62 and cleaved caspase-3 levels in a time-dependent manner during renal I/R injury, as well as increased the number of intracellular double-membrane vesicles in injured renal cells. IPC-induced renal protection was efficiently attenuated by pretreatment with 5 mM 3-MA. Pretreatment with IPC also dynamically affected the expression of SGK1/FOXO3a/HIF-1α signaling components. Moreover, knocking down SGK1 expression significantly downregulated phosphorylated-FOXO3a (p-FOXO3a)/FOXO3 and HIF-1α, suppressed LC3II and Beclin-1 levels, increased SQSTM/p62 and cleaved caspase-3 levels, and abolished the protective effect of IPC against I/R-induced renal damage. SGK1 overexpression efficiently increased p-FOXO3a/FOXO3 and HIF-1α levels, promoted the autophagy flux and enhanced the protective effect mediated by HPC. Furthermore, FOXO3a overexpression decreased HIF-1α protein levels, inhibited HIF-1α transcriptional activity and reduced the protective effect of IPC. Our study indicates that IPC can ameliorate renal I/R injury by promoting autophagy through the SGK1 pathway.

Indexed as

AutophagyAnimalsBeclin-1Forkhead Box Protein O3HumansHypoxia-Inducible Factor 1, alpha SubunitImmediate-Early ProteinsIschemic PreconditioningKidneyKidney DiseasesMaleMicrotubule-Associated ProteinsProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyReperfusion InjuryAnxa3 protein, ratBeclin-1Forkhead Box Protein O3FOXO3 protein, ratHypoxia-Inducible Factor 1, alpha SubunitImmediate-Early ProteinsMicrotubule-Associated ProteinsProtein Serine-Threonine KinasesSequestosome-1 ProteinSerum-Glucocorticoid Regulated KinasesSqstm1 protein, rat

Identifiers

PMID29497029
PMCPMC5832808
OpenAlexW2791743420

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.