Evidence map›Paper›PMID 29179471›Full record

ArticleOncotarget2017

Histone deacetylase 6 inhibition counteracts the epithelial-mesenchymal transition of peritoneal mesothelial cells and prevents peritoneal fibrosis.

Liuqing Xu, Na Liu, Hongwei Gu, Hongrui Wang, Yingfeng Shi, Xiaoyan Ma, Shuchen Ma, Jun Ni, Min Tao, Andong Qiu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 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

11 authors at 3 institutions in 2 countries.

Liuqing XuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Na LiuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Hongwei GuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Hongrui WangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yingfeng ShiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaoyan MaDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shuchen MaDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jun NiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Min TaoDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Andong QiuSchool of Life Sciences and Technology, Advanced Institute of Translational Medicine, Tongji University, Shanghai, China.
Shougang ZhuangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shanghai East Hospital · CNBrown University · USTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of histone deacetylase 6 (HDAC6) in peritoneal fibrosis remains unknown. In this study, we examined the effect of HDAC6 inhibition on the epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells and development of peritoneal fibrosis. Treatment with tubastatin A, a highly selective HDAC6 inhibitor, or silencing of HDAC6 with siRNA inhibited transforming growth factor β1-induced EMT, as evidenced by decreased expression of α-smooth muscle actin, collagen I and preserved expression of E-cadherin in cultured human peritoneal mesothelial cells. In a mouse model of peritoneal fibrosis induced by high glucose dialysate, administration of TA prevented thickening of the submesothelial region and decreased expression of collagen I and α-SMA. Mechanistically, tubastatin A treatment inhibited expression of TGF-β1 and phosphorylation of Smad-3, epidermal growth factor receptor, STAT3, and NF-κBp65. HDAC6 inhibition also suppressed production of multiple inflammatory cytokines/chemokines and reduced the infiltration of macrophages to the injured peritoneum. Moreover, tubastatin A was effective in inhibiting peritoneal increase of CD31(+) blood vessels and expression of vascular endothelial growth factor in the injured peritoneum. Collectively, these results suggest that HDAC6 inhibition can attenuate peritoneal fibrosis by inhibiting multiple pro-fibrotic signaling pathways, EMT, inflammation and blood vessel formation.

Indexed as

HDAC6inflammationperitoneal fibrosisTGF-β signaling pathwayvascular endothelial growth factor

Identifiers

PMID29179471
PMCPMC5687641
OpenAlexW2754900008

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.