Evidence map›Paper›PMID 29233979›Full record

ArticleCell death & disease2017

Extracellular vesicles from human-induced pluripotent stem cell-derived mesenchymal stromal cells (hiPSC-MSCs) protect against renal ischemia/reperfusion injury via delivering specificity protein (SP1) and transcriptional activating of sphingosine kinase 1 and inhibiting necroptosis.

Xiaodong Yuan, Dawei Li, Xiaosong Chen, Conghui Han, Longmei Xu, Tao Huang, Zhen Dong, Ming Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 2 syntheses or guidelines pooled it, 150 citations in OpenAlex.

  1. Pooled it
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  10. Function ofOncology letters · 2025
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  16. Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025
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23 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 1 country.

Xiaodong YuanDepartment of Transplantation and Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Dawei LiDepartment of Transplantation and Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiaosong ChenDepartment of Hepatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Conghui HanDepartment of Urology, Xuzhou Central Hospital, Xuzhou Medical University School of Clinical Medicine, Xuzhou, China.
Longmei XuThe Animal Facility of Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Tao HuangTransplantation Center of the Affiliated Hospital of Qingdao University, Qingdao, China.
Zhen DongTransplantation Center of the Affiliated Hospital of Qingdao University, Qingdao, China.
Ming ZhangDepartment of Transplantation and Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. drmingzhang@126.com.
Shanghai Jiao Tong University · CNAffiliated Hospital of Qingdao University · CNRenji Hospital · CNXuzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischemia-reperfusion is a main cause of acute kidney injury (AKI), which is associated with high mortality. Here we show that extracellular vesicles (EVs) secreted from hiPSC-MSCs play a critical role in protection against renal I/R injury. hiPSC-MSCs-EVs can fuse with renal cells and deliver SP1 into target cells, subsequently active SK1 expression and increase S1P formation. Chromatin immunoprecipitation (ChIP) analyses and luciferase assay were used to confirm SP1 binds directly to the SK1 promoter region and promote promoter activity. Moreover, SP1 inhibition (MIT) or SK1 inhibition (SKI-II) completely abolished the renal protective effect of hiPSC-MSCs-EVs in rat I/R injury mode. However, pre-treatment of necroptosis inhibitor Nec-1 showed no difference with the administration of hiPSC-MSCs-EVs only. We then generated an SP1 knockout hiPSC-MSC cell line by CRISPR/Cas9 system and found that SP1 knockout failed to show the protective effect of hiPSC-MSCs-EVs unless restoring the level of SP1 by Ad-SP1 in vitro and in vivo. In conclusion, this study describes an anti-necroptosis effect of hiPSC-MSCs-EVs against renal I/R injury via delivering SP1 into target renal cells and intracellular activating the expression of SK1 and the generation of S1P. These findings suggest a novel mechanism for renal protection against I/R injury, and indicate a potential therapeutic approach for a variety of renal diseases and renal transplantation.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCell DifferentiationCell Line, TransformedEpithelial CellsExtracellular VesiclesGene Expression RegulationHumansInduced Pluripotent Stem CellsKidneyLysophospholipidsMaleMesenchymal Stem CellsNecrosisPhosphotransferases (Alcohol Group Acceptor)LysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Sp1 Transcription FactorSphingosinesphingosine 1-phosphateSphingosine Kinase

Identifiers

PMID29233979
PMCPMC5870585
OpenAlexW2775012345

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.