Evidence map›Paper›PMID 31427681›Full record

ArticleScientific reports2019

The p21 dependent G2 arrest of the cell cycle in epithelial tubular cells links to the early stage of renal fibrosis.

Takayuki Koyano, Masumi Namba, Tomoe Kobayashi, Kyomi Nakakuni, Daisuke Nakano, Masaki Fukushima, Akira Nishiyama, Makoto Matsuyama

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Tubular FoxP2 and Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025
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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

8 authors at 2 institutions in 1 country.

Takayuki KoyanoDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.ORCID http://orcid.org/0000-0003-1675-2525
Masumi NambaDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Tomoe KobayashiDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Kyomi NakakuniShigei Medical Research Hospital, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Daisuke NakanoDepartment of Pharmacology, Kagawa University Medical School, 1750-1 Ikenobe, Miki-cho, Kagawa, 761-0793, Japan.
Masaki FukushimaDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Akira NishiyamaDepartment of Pharmacology, Kagawa University Medical School, 1750-1 Ikenobe, Miki-cho, Kagawa, 761-0793, Japan.
Makoto MatsuyamaDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan. matsuyama@shigei.or.jp.
Shigei Medical Research Institute · JPKagawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is accompanied by the progression of chronic kidney disease. Despite a number of past and ongoing studies, our understanding of the underlying mechanisms remains elusive. Here we explored the progression of renal fibrosis using a mouse model of unilateral ureter obstruction. We found that in the initial stage of damage, where extracellular matrix was not yet deposited, proximal tubular cells arrested at G2 of the cell cycle. Further analyses indicated that the cyclin-dependent kinase inhibitor p21 is partially involved in the G2 arrest after the damage. A newly produced monoclonal antibody against p21 revealed that levels of p21 were sharply upregulated in response to the damage during the initial stage but dropped toward the later stage. To investigate the requirement of p21 for the progression of renal fibrosis, we constructed the novel p21 deficient mice by i-GONAD method. Compared with wild-type mice, p21 deficient mice showed exacerbation of the fibrosis. Thus we propose that during the initial stage of the renal damage, tubular cells arrest in G2 partially depending on p21, thereby safeguarding kidney functions.

Indexed as

AnimalsBiomarkersCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease SusceptibilityDNA DamageEpithelial CellsFibrosisFluorescent Antibody TechniqueG2 Phase Cell Cycle CheckpointsKidney DiseasesKidney TubulesMiceSeverity of Illness IndexBiomarkersCyclin-Dependent Kinase Inhibitor p21

Identifiers

PMID31427681
PMCPMC6700145
OpenAlexW2968770226

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.