Evidence map›Paper›PMID 30429495›Full record

ArticleScientific reports2018

Radiation-induced premature cellular senescence involved in glomerular diseases in rats.

Sae Aratani, Masako Tagawa, Shinya Nagasaka, Yukinao Sakai, Akira Shimizu, Shuichi Tsuruoka

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Sae ArataniDepartment of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan. sae-aratani@nms.ac.jp.ORCID http://orcid.org/0000-0002-5581-2618
Masako TagawaDepartment of Analytic Human Pathology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Shinya NagasakaDepartment of Analytic Human Pathology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Yukinao SakaiDepartment of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Akira ShimizuDepartment of Analytic Human Pathology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Shuichi TsuruokaDepartment of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Nippon Medical School · JPNippon Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, cellular senescence has emerged as a fundamental contributor to chronic organ diseases. Radiation is one of the stress factors that induce cellular senescence. Although the kidney is known as a radiosensitive organ, whether and how radiation-induced cellular senescence is associated with kidney diseases remains unclear. In this study, we performed experiments on 7-8-week-old male rats that received a single dose of 18-Gy radiation in the unilateral kidney. The irradiated kidneys showed hallmarks of cellular senescence, including increased SA-β-gal activity, upregulation of cyclin-dependent kinase inhibitor (p53, p21, and p16), and absence of DNA proliferation marker (Ki-67). Furthermore, combined with in-vitro experiments, we demonstrated that radiation-induced senescent glomerular endothelial cells acquired altered gene expression, namely, senescence-associated secretory phenotype (particularly, IL-6), which might be triggered by NF-kB signaling pathway. Pathological analysis suggested severe glomerular endothelial cell injury, as evidenced by thrombotic microangiopathy, collapsing glomeruli, and reduced endothelial cell numbers. We suggested that glomerular endothelial cells were more susceptible to radiation-induced cellular senescence. In conclusion, the current study is the first to identify the important role of radiation-induced cellular senescence, mainly derived from glomerular endothelial cells, for the development of glomerular injury.

Indexed as

AnimalsCellular SenescenceEndothelial CellsGene Expression RegulationKidney DiseasesKidney GlomerulusMaleRadiation Injuries, ExperimentalRatsX-Rays

Identifiers

PMID30429495
PMCPMC6235850
OpenAlexW2899962460

What OpenQuestion holds

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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.