Evidence map›Paper›PMID 36883358›Full record

ArticleRenal failure2023

Mesenchymal stem cells protect against sepsis-associated acute kidney injury by inducing Gal-9/Tim-3 to remodel immune homeostasis.

Congjuan Luo, Feng Luo, Lin Che, Hui Zhang, Long Zhao, Wei Zhang, Xiaofei Man, Quandong Bu, Hong Luan, Bin Zhou and 2 more

Open access · goldFull text read
In one paragraph

Article in Renal failure, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. TIM-3, a potential target for sepsis therapy.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
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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

12 authors at 2 institutions in 1 country.

Congjuan LuoDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Feng LuoDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Lin CheDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Hui ZhangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Long ZhaoDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Wei ZhangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Xiaofei ManDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Quandong BuDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Hong LuanDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Bin ZhouDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Haiyan ZhouDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Yan XuDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe present study investigated the specific mechanism by which mesenchymal stem cells (MSCs) protect against sepsis-associated acute kidney injury (SA-AKI).

methodsMale C57BL/6 mice underwent cecal ligation and puncture surgery to induce sepsis and then received either normal IgG or MSCs (1 × 10

resultsAfter cecal ligation and puncture surgery, the mice injected with Gal-9 or MSCs plus Gal-9 had a higher survival rate than the mice in the IgG treatment group. Treatment with MSCs plus Gal-9 decreased serum creatinine and blood urea nitrogen levels, improved tubular function recovery, reduced IL-17 and RORγt levels and induced IL-10 and FOXP3 expression. Additionally, the Th17/Treg cell balance was altered. However, when soluble Tim-3 was used to block the Gal-9/Tim-3 pathway, the septic mice developed kidney injury and exhibited increased mortality. Treatment with MSCs plus soluble Tim-3 blunted the therapeutic effect of MSCs, inhibited the induction of Tregs, and suppressed the inhibition of differentiation into Th17 cells.

conclusionTreatment with MSCs significantly reversed the Th1/Th2 balance. Thus, the Gal-9/Tim-3 pathway may be an important mechanism of MSC-mediated protection against SA-AKI.

Indexed as

Acute Kidney InjuryHomeostasisMesenchymal Stem CellsSepsisAnimalsForkhead Transcription FactorsGalectinsHepatitis A Virus Cellular Receptor 2Immunoglobulin GInterleukin-10Interleukin-17MaleMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLNuclear Receptor Subfamily 1, Group F, Member 3Forkhead Transcription FactorsFoxp3 protein, mousegalectin 9, mouseGalectinsHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2IL10 protein, mouseIl17a protein, mouseImmunoglobulin GInterleukin-10Interleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3Gal-9/Tim-3immune homeostasisMesenchymal stem cellssepsis-associated acute kidney injury

Identifiers

PMID36883358
PMCPMC10013538
OpenAlexW4323532737

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Textfull text, public
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.