Evidence map›Paper›PMID 27270990›Full record

ArticleScientific reports2016

Inhibition of microtubule dynamics impedes repair of kidney ischemia/reperfusion injury and increases fibrosis.

Sang Jun Han, Ji-Hyeon Kim, Jee In Kim, Kwon Moo Park

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

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  14. Histone acetylation and DNA methylation in ischemia/reperfusion injury.Clinical science (London, England : 1979) · 2019
    Review
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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

4 authors at 2 institutions in 1 country.

Sang Jun HanDepartment of Anatomy, Cardiovascular Research Institute, and BK21 Plus, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
Ji-Hyeon KimDepartment of Anatomy, Cardiovascular Research Institute, and BK21 Plus, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
Jee In KimDepartment of Molecular Medicine and MRC, College of Medicine, Keimyung University, Daegu 704-701, Republic of Korea.
Kwon Moo ParkDepartment of Anatomy, Cardiovascular Research Institute, and BK21 Plus, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
Keimyung University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microtubule cytoskeleton is composed of α-tubulin and β-tubulin heterodimers, and it serves to regulate the shape, motility, and division of a cell. Post-translational modifications including acetylation are closely associated with the functional aspects of the microtubule, involving in a number of pathological diseases. However, the role of microtubule acetylation in acute kidney injury (AKI) and progression of AKI to chronic kidney disease have yet to be understood. In this study, ischemia/reperfusion (I/R), a major cause of AKI, resulted in deacetylation of the microtubules with a decrease in α-tubulin acetyltransferase 1 (α-TAT1). Paclitaxel (taxol), an agent that stabilizes microtubules by tubulin acetylation, treatment during the recovery phase following I/R injury inhibited tubular cell proliferation, impaired renal functional recovery, and worsened fibrosis. Taxol induced α-tubulin acetylation and post-I/R cell cycle arrest. Taxol aggregated the microtubule in the cytoplasm, resulting in suppression of microtubule dynamics. Our studies have demonstrated for the first time that I/R induced deacetylation of the microtubules, and that inhibition of microtubule dynamics retarded repair of injured tubular epithelial cells leading to an acceleration of fibrosis. This suggests that microtubule dynamics plays an important role in the processes of repair and fibrosis after AKI.

Indexed as

Wound HealingAcetylationAnimalsCell Cycle CheckpointsCell ProliferationCheckpoint Kinase 2ColchicineDisease ProgressionEpithelial CellsFibrosisKidneyMacrophagesMaleMiceMicrotubulesMonocytesCheckpoint Kinase 2Chek2 protein, mouseColchicinePaclitaxelTubulin

Identifiers

PMID27270990
PMCPMC4897697
OpenAlexW2418705080

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.