Evidence map›Paper›PMID 29130363›Full record

ArticleAutophagy2018

Antioxidant role of autophagy in maintaining the integrity of glomerular capillaries.

Jun Matsuda, Tomoko Namba, Yoshitsugu Takabatake, Tomonori Kimura, Atsushi Takahashi, Takeshi Yamamoto, Satoshi Minami, Shinsuke Sakai, Ryuta Fujimura, Jun-Ya Kaimori and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
4.1field-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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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  18. Autophagy and Renal Fibrosis.Aging and disease · 2022
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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

16 authors at 3 institutions in 1 country.

Jun Matsudaa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Tomoko Nambaa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.ORCID 0000-0002-6049-7616
Yoshitsugu Takabatakea Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.ORCID 0000-0002-8912-2316
Tomonori Kimuraa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Atsushi Takahashia Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Takeshi Yamamotoa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Satoshi Minamia Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Shinsuke Sakaia Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Ryuta Fujimuraa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Jun-Ya Kaimorib Department of Advanced Technology for Transplantation , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Isao Matsuia Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.ORCID 0000-0001-8378-6130
Takayuki Hamanoc Department of Comprehensive Kidney Disease Research (CKDR) , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Yoko Fukushimad Department of Ophthalmology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
Keiko Matsuie Department of Hematology and Oncology , Tokai University School of Medicine , 143 Shimokasuya, Isehara , Kanagaw , Japan.
Tomoyoshi Sogaf Institute for Advanced Biosciences , Keio University , Tsuruoka , Yamagata , Japan.
Yoshitaka Isakaa Department of Nephrology , Osaka University Graduate School of Medicine , 2-2 Yamada-oka, Suita , Osaka , Japan.
The University of Osaka · JPKeio University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a lysosomal degradation system by which cytosolic materials and damaged organelles are broken down into basic components. To explore the physiological role of autophagy in glomerular endothelial cells (GEnCs), we compared the autophagic flux among cells in the kidney under starvation. Inhibition of autophagy by chloroquine administration significantly increased the number of autophagosomes or autolysosomes in GEnCs and proximal tubular cells, but not in podocytes, suggesting that the GEnCs exhibit substantial autophagic activity. Next, we analyzed endothelial and hematopoietic cell-specific atg5-deficient mice (atg5-conditional KO [cKO] mice). Glomeruli of 4-wk-old atg5-cKO mice exhibited slightly distended capillary loops accompanied by an accumulation of reactive oxygen species (ROS). Glomeruli of 8-wk-old atg5-cKO mice showed a lobular pattern with thickening of the capillary loops and mesangial matrix expansion; however, the vasculature of other organs was preserved. The atg5-cKO mice died by 12 wk of age, presumably due to pancytopenia resulting from the defect in their hematopoietic lineages. Therefore, we subjected 4-wk atg5-cKO mice to irradiation followed by bone marrow transplantation from normal littermates. Transplanted mice recapitulated the glomerular phenotypes of the atg5-cKO mice with no obvious histological changes in other organs. Twelve-mo-old transplanted mice developed mesangiolysis and glomerulosclerosis with significant deterioration of kidney function. Administration of N-acetyl-l-cysteine, a ROS scavenger, to atg5-cKO mice rescued the glomerular phenotypes. These data suggest that endothelial autophagy protects glomeruli from oxidative stress and maintains the integrity of glomerular capillaries. Enhancing endothelial autophagy may provide a novel therapeutic approach to minimizing glomerular diseases.

Indexed as

AnimalsAntioxidantsAutophagyAutophagy-Related Protein 5CapillariesCells, CulturedChloroquineEndothelial CellsHumansKidney DiseasesKidney GlomerulusMiceMice, KnockoutOxidative StressReactive Oxygen SpeciesAntioxidantsAtg5 protein, mouseAutophagy-Related Protein 5ChloroquineReactive Oxygen SpeciesAtg5autophagic fluxautophagyglomerular endothelial cellsoxidative stress

Identifiers

PMID29130363
PMCPMC5846506
OpenAlexW2768621718

What OpenQuestion holds

Textmetadata
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.