Evidence map›Paper›PMID 33015978›Full record

ArticleBasic & clinical pharmacology & toxicology2021

Thal protects against paraquat-induced lung injury through a microRNA-141/HDAC6/IκBα-NF-κB axis in rat and cell models.

Fenshuang Zheng, Junbo Zhu, Wei Zhang, Yangshan Fu, Zhaoheng Lin

Open access · hybridAbstract read
In one paragraph

Article in Basic & clinical pharmacology & toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. Article
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

5 authors at 1 institution in 1 country.

Fenshuang ZhengDepartment of Emergency Medicine, Second People's Hospital of Yunnan Province, Kunming, China.
Junbo ZhuDepartment of Emergency Medicine, Second People's Hospital of Yunnan Province, Kunming, China.
Wei ZhangDepartment of Emergency Medicine, Second People's Hospital of Yunnan Province, Kunming, China.
Yangshan FuDepartment of Emergency Medicine, Second People's Hospital of Yunnan Province, Kunming, China.
Zhaoheng LinDepartment of Critical Care Medicine, People's Hospital of Xishuangbanna Dai Nationality Autonomous Prefecture, Pingpong, China.ORCID https://orcid.org/0000-0002-6488-8147
Second People's Hospital of Yunnan Province · CN

Funding

Key project of Kunming Science and Technology Plan: Basic and Clinical Study on Thalidomide in the Treatment of Paraquat Poisoning Lung Injury 2015-2-S-01408
6 · The paper itself

Abstract

The protective functions of thalidomide in paraquat (PQ)-induced injury have been reported. But the mechanisms remain largely unknown. In this research, a PQ-treated rat model was established and further treated with thalidomide. Oedema and pathological changes, oxidative stress, inflammation, fibrosis and cell apoptosis in rat lungs were detected. A PQ-treated RLE-6TN cell model was constructed, and the viability and apoptosis rate of cells were measured. Differentially expressed microRNAs (miRNAs) after thalidomide administration were screened out. Binding relationship between miR-141 and histone deacetylase 6 (HDAC6) was validated. Altered expression of miR-141 and HDAC6 was introduced to identify their involvements in thalidomide-mediated events. Consequently, thalidomide administration alone exerted no damage to rat lungs; in addition it reduced PQ-induced oedema. The oxidative stress, inflammation and cell apoptosis in rat lungs were reduced by thalidomide. In RLE-6TN cells, thalidomide increased cell viability and decreased apoptosis. miR-141 was responsible for thalidomide-mediated protective events by targeting HDAC6. Overexpression of HDAC6 blocked the protection of thalidomide against PQ-induced injury via activating the IkBα-NF-κB signalling pathway. Collectively, this study evidenced that thalidomide protects lung tissues from PQ-induced injury through a miR-141/HDAC6/IkBα-NF-κB axis.

Indexed as

AnimalsApoptosisCell LineDisease Models, AnimalFemaleHistone Deacetylase 6Inflammation MediatorsLungLung InjuryMicroRNAsNF-kappa BNF-KappaB Inhibitor alphaOxidative StressParaquatProtective AgentsPulmonary EdemaHDAC6 protein, ratHistone Deacetylase 6Inflammation MediatorsMicroRNAsMirn141 microRNA, ratNF-kappa BNF-KappaB Inhibitor alphaParaquatProtective AgentsThalidomidegene expressionlung injuryParaquatrisk assessmentthalidomideviabilityWistar rat

Identifiers

PMID33015978
PMCPMC7894280
OpenAlexW3091191281

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.