Evidence map›Paper›PMID 16436654›Full record

ArticleThe American journal of pathology2006

Autophagic cardiomyocyte death in cardiomyopathic hamsters and its prevention by granulocyte colony-stimulating factor.

Shusaku Miyata, Genzou Takemura, Yukinori Kawase, Yiwen Li, Hideshi Okada, Rumi Maruyama, Hiroaki Ushikoshi, Masayasu Esaki, Hiromitsu Kanamori, Longhu Li and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 111 citations in OpenAlex.

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  12. Lipotoxic very-long-chain ceramides cause mitochondrial dysfunction, oxidative stress, and cell death in cardiomyocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
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  19. G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice.Laboratory investigation; a journal of technical methods and pathology · 2015
    Article
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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.

Shusaku MiyataSecond Department of Internal Medicine, Gifu University School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan.
Genzou Takemura
Yukinori Kawase
Yiwen Li
Hideshi Okada
Rumi Maruyama
Hiroaki Ushikoshi
Masayasu Esaki
Hiromitsu Kanamori
Longhu Li
Yu Misao
Asaki Tezuka
Teruhiko Toyo-Oka
Shinya Minatoguchi
Takako Fujiwara
Hisayoshi Fujiwara
Gifu University · JPThe University of Tokyo · JPKyoto Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In UM-X7.1 hamster model of human dilated cardiomyopathy, heart failure progressively develops and causes 50% mortality by 30 weeks of age. Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen granules, and myelin-like figures. In addition, ubiquitin, cathepsin D, and Rab7 were overexpressed as determined by immunoassays. Importantly, most cardiomyocytes with leaky plasma membranes were positive for cathepsin D, suggesting a direct link between autophagic degeneration and cell death. Meanwhile, cardiomyocyte apoptosis appeared insignificant. Granulocyte colony-stimulating factor (10 microg/kg/day), injected 5 days/week from 15 to 30 weeks of age, improved survival among 30-week-old hamsters (100% versus 53% in the untreated hamsters, P < 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colony-stimulating factor also down-regulated tumor necrosis factor-alpha and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. In conclusion, autophagic death is important for cardiomyocyte loss in the cardiomyopathic hamster, and the beneficial effect of granulocyte colony-stimulating factor acts mainly via an anti-autophagic mechanism rather than anti-apo-ptosis or regeneration.

Indexed as

ApoptosisAutophagyAnimalsCardiomyopathy, DilatedCathepsin DCricetinaeFibrosisGranulocyte Colony-Stimulating FactorMaleMesocricetusMitochondriaMyelin SheathMyocytes, CardiacProto-Oncogene Proteins c-aktrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsCathepsin DGranulocyte Colony-Stimulating FactorProto-Oncogene Proteins c-aktrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, humanrab GTP-Binding ProteinsRecombinant ProteinsSTAT3 Transcription FactorTumor Necrosis Factor-alphaUbiquitin

Identifiers

PMID16436654
PMCPMC1606501
OpenAlexW2119299191

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.