Evidence map›Paper›PMID 32312307›Full record

ArticleJournal of translational medicine2020

High-mobility group box 1 protein antagonizes the immunosuppressive capacity and therapeutic effect of mesenchymal stem cells in acute kidney injury.

Shuo Wang, Songjie Cai, Weitao Zhang, Xigao Liu, Yan Li, Chao Zhang, Yigang Zeng, Ming Xu, Ruiming Rong, Tianshu Yang and 4 more

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

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. A WR3-NHMaterials today. Bio · 2026
    Article
  3. Article
  4. Article
  5. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
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  7. Article
  8. Review
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

14 authors at 7 institutions in 2 countries.

Shuo WangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Songjie CaiTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave, LRMC 301, Boston, MA, 02115, USA.
Weitao ZhangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Xigao LiuDepartment of Urology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Yan LiDepartment of Urology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Chao ZhangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Yigang ZengDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Ming XuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Ruiming RongDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China.
Tianshu YangShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Benkang ShiDepartment of Urology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Anil ChandrakerTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave, LRMC 301, Boston, MA, 02115, USA. achandraker@bwh.harvard.edu.
Cheng YangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China. esuperyc@163.com.
Tongyu ZhuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai Key Laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai, 200032, China. tyzhu@fudan.edu.cn.
Zhongshan Hospital · CNQilu Hospital of Shandong University · CNFudan University · CNShanghai Public Health Clinical Center · CNBrigham and Women's Hospital · USHarvard University · USTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKidney ischemia reperfusion injury (IRI) is a common cause of acute kidney injury and an unavoidable consequence of kidney transplantation and still lacks specific therapeutics. Recently, mesenchymal stem cell (MSC) has been emerging as a promising cell-based therapy for IRI in the context of transplantation. MSC negatively regulates the secretion of pro-inflammatory as well as the activation of immune cells during IRI through its unique immunosuppressive property.

methodsWe employed mice kidney IRI model and MSC cell line to monitor the IRI related checkpoints. siRNAs were utilized to knock down the potential key factors for mechanistic analysis. Statistical analysis was performed by using one-way ANOVA with Tukey's post hoc procedure by SPSS.

resultsThe expression of high-mobility group box 1 protein (HMGB1) is increased in the acute phase as well as the recovery stage of IRI. Importantly, the HMGB1 upregulation is correlated with the injury severity. HMGB1 diminishes the MSC induced immunosuppressive capacity in the presence of pro-inflammatory cytokines in vitro. Toll like receptor 4 (TLR4)-mediated inducible nitric oxide synthase (iNOS) inhibition contributes to the negative effect of HMGB1 on MSCs. HMGB1-TLR4 signaling inhibition augments the therapeutic efficacy of MSCs in mice renal IRI model.

conclusionsThese findings demonstrate that HMGB1 plays a crucial role in shaping the immunoregulatory property of MSCs within the microenvironments, providing novel insights into the crosstalk between MSCs and microenvironment components, suggesting HMGB1 signals as a promising target to improve MSC-based therapy.

Indexed as

Acute Kidney InjuryHMGB1 ProteinMesenchymal Stem CellsReperfusion InjuryAnimalsKidneyMiceHMGB1 ProteinHMGB1 protein, mouseAcute kidney injuryCell therapyHMGB1Ischemia–reperfusion injuryMesenchymal stem cell

Identifiers

PMID32312307
PMCPMC7169035
OpenAlexW3016653516

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.