Evidence map›Paper›PMID 29348412›Full record

ArticleScientific reports2018

Influence of autophagy on acute kidney injury in a murine cecal ligation and puncture sepsis model.

Satoshi Sunahara, Eizo Watanabe, Masahiko Hatano, Paul E Swanson, Takehiko Oami, Lisa Fujimura, Youichi Teratake, Takashi Shimazui, Chiwei Lee, Shigeto Oda

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.2field-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

43 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  3. From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 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

10 authors at 3 institutions in 2 countries.

Satoshi SunaharaDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Eizo WatanabeDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. watanabee@faculty.chiba-u.jp.ORCID http://orcid.org/0000-0001-6731-909X
Masahiko HatanoBiomedical Research Center, Chiba University, Chiba, Japan.
Paul E SwansonDepartment of Pathology, University of Washington School of Medicine, Seattle, USA.
Takehiko OamiDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0003-2630-7716
Lisa FujimuraBiomedical Research Center, Chiba University, Chiba, Japan.
Youichi TeratakeBiomedical Research Center, Chiba University, Chiba, Japan.
Takashi ShimazuiDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiwei LeeDepartment of Nephrology, Chiba University Graduate School of Medicine, Chiba, Japan.
Shigeto OdaDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University · JPChiba University Hospital · JPUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of autophagy in the maintenance of renal homeostasis during sepsis is not well understood. We therefore aimed to determine the influence of autophagy on kidney during sepsis using a murine sepsis model, i.e. cecal ligation and puncture (CLP). In CLP treated animals, the number of autolysosomes observed by electron microscopy increased over time. The number of autophagosomes in CLP animals decreased relative sham operated controls at 24 hrs after CLP, indicating that autophagy flux is already diminishing by that time. Moreover, CLP induced an increase in LC3-II/LC3-I ratio at 6-8 hrs, demonstrated in western blots, as well as an increase in GFP-LC3 dots at 6-8 hrs and 24 hrs, using immunofluorescence and anti-LC3 and LAMP1 antibodies on tissue sections from GFP-LC3 transgenic mice. LC3-II/LC3-I ratio and the number of co-localized GFP-LC3 dots and LAMP1 signals (GFP LC3 + LAMP1 dots) in CLP mice at 24 hrs were significantly reduced compared with data obtained at 6-8 hrs. Notably, acceleration of autophagy by rapamycin resulted in improvement of renal function that was associated with improvement in the histologic severity of tubular epithelial injury in CLP treated animals. Autophagy in the kidney was significantly slowed in the kidney during the acute phase of sepsis; nonetheless, autophagy in kidney appears to play a protective role against sepsis.

Indexed as

AutophagyAcute Kidney InjuryAnimalsAutophagosomesDisease Models, AnimalKidneyLysosomesMaleMiceSepsis

Identifiers

PMID29348412
PMCPMC5773584
OpenAlexW2784238814

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.