Evidence map›Paper›PMID 27747000›Full record

ArticleJournal of thoracic disease2016

Suberoylanilide hydroxamic acid attenuates paraquat-induced pulmonary fibrosis by preventing Smad7 from deacetylation in rats.

Shan-Shan Rao, Xiang-Yan Zhang, Ming-Jun Shi, Ying Xiao, Ying-Ying Zhang, Yuan-Yuan Wang, Chang-Zhi Zhang, Song-Jun Shao, Xin-Mei Liu, Bing Guo

Open access · hybridAbstract read
In one paragraph

Article in Journal of thoracic disease, 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, 30 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

10 authors at 2 institutions in 1 country.

Shan-Shan RaoDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Xiang-Yan ZhangDepartment of Respiratory Medicine, The People's Hospital of Guizhou Province, Guiyang 550025, China;; Academic Department, Guizhou Institute of Respiratory Diseases, Guiyang 55002, China.
Ming-Jun ShiDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Ying XiaoDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Ying-Ying ZhangDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Yuan-Yuan WangDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Chang-Zhi ZhangDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Song-Jun ShaoDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Xin-Mei LiuDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Bing GuoDepartment of Pathophysiology, Guizhou Medical University, Guiyang 550025, China.
Guiyang Medical University · CNGuizhou Institute of Biology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent evidence suggests that a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), has anti-fibrotic effect. However, the exact mechanism of its anti-fibrotic potential remains is unclear. In this study, we investigated the molecular mechanism of SAHA in attenuating pulmonary fibrosis by regulating stability of Smad7 in paraquat (PQ)-induced lung fibrosis animal model and cultured pulmonary fibroblasts.

methodsRats with paraquat-induced lung fibrosis were fed with a SAHA solution (15 mg/kg) by gastric gavage. Human pulmonary fibroblasts (HFL1) pre-treated with TGF-β1 (5 ng/mL) were treated with SAHA (5 µM).

resultsSAHA (histone deacetylase inhibitor, HDACi) suppressed PQ-induced lung fibrosis in rats by stabilizing Smad7 level, thus attenuating Smad3 activity, resulting in the inhibition of fibroblast differentiation and collagen expression. In vitro study showed that SAHA suppressed TGF-β1-induced fibroblast differentiation into myofibroblasts. SAHA exerted its antifibrotic effect through preventing Smad7 from deacetylation most maybe by inhibiting TGF-β1-induced HDAC1 activity.

conclusionsSAHA repressed PQ-induced lung fibrosis via preventing Smad7 from deacetylation.

Indexed as

histone deacetylase 1 (HDAC1)Pulmonary fibrosisSmad7 acetylationsuberoylanilide hydroxamic acid (SAHA)TGF-β1

Identifiers

PMID27747000
PMCPMC5059239
OpenAlexW2521031097

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.