Evidence map›Paper›PMID 33475136›Full record

ArticleJournal of molecular cell biology2021

Testosterone attenuates pulmonary epithelial inflammation in male rats of COPD model through preventing NRF1-derived NF-κB signaling.

Xueting Wang, Linlin Huang, Shan Jiang, Kang Cheng, Dan Wang, Qianqian Luo, Xiaomei Wu, Li Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 9% 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, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  14. Review
  15. Testosterone attenuates hypoxia-induced hypertension by affecting NRF1-mediated transcriptional regulation of ET-1 and ACE.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  16. Whole-Exome Sequencing Implicates theFrontiers in cell and developmental biology · 2021
    Article
  17. Testosterone in COVID-19: An Adversary Bane or Comrade Boon.Frontiers in cellular and infection microbiology · 2021
    Review
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 1 institution in 1 country.

Xueting WangInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Linlin HuangInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Shan JiangInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Kang ChengInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Dan WangInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Qianqian LuoInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Xiaomei WuInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Li ZhuInstitute of Special Environmental Medicine, Nantong University, Nantong 226019, China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Testosterone deficiency is common in male patients with chronic obstructive pulmonary disease (COPD) and may correlate with the deterioration of COPD. Clinical research suggests that testosterone replacement therapy may slow the COPD progression, but the specific biological pathway remains unclear. In this study, we explored the effect of testosterone on pulmonary inflammation in male COPD rats. The animals were co-treated with lipopolysaccharide (LPS) and cigarette to induce COPD. In COPD rats, nuclear respiratory factor 1 (NRF1) and NF-κB p65 were upregulated. In cigarette smoke extract (CSE)-, LPS-, or the combination of CSE and LPS-treated L132 cells, NRF1 and p65 were also upregulated. Silencing NRF1 resulted in the downregulation of p65. ChIP‒seq, ChIP‒qPCR, and luciferase results showed that NRF1 transcriptionally regulated p65. Both male and female COPD rats showed an upregulated NRF1 level and similar pulmonary morphology. But NRF1 was further upregulated in male castrated rats. Further supplementing testosterone in castrated male rats significantly reduced NRF1, pulmonary lesions, and inflammation. Supplementation of testosterone also reduced the phosphorylation of p65 and IKKβ induced by LPS or CSE in L132 cells. Our results suggest that testosterone plays a protective role in pulmonary epithelial inflammation of COPD through inhibition of NRF1-derived NF-κB signaling and the phosphorylation of p65.

Indexed as

Signal TransductionAnimalsBiomarkersDisease Models, AnimalDisease SusceptibilityFemaleGene ExpressionImmunohistochemistryLipopolysaccharidesMaleNF-kappa BNuclear Respiratory Factor 1OrchiectomyPulmonary AlveoliPulmonary Disease, Chronic ObstructiveRatsBiomarkersLipopolysaccharidesNF-kappa BNuclear Respiratory Factor 1SmokeTestosteroneTranscription Factor RelACOPDendotheliaNF-κBNRF1testosterone replacement therapytranscriptional regulation

Identifiers

PMID33475136
PMCPMC8104951
OpenAlexW3122808906

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.