Evidence map›Paper›PMID 34414534›Full record

ArticleInflammation2022

Thymosin β4 Suppresses LPS-Induced Murine Lung Fibrosis by Attenuating Oxidative Injury and Alleviating Inflammation.

Zhen Tian, Naijuan Yao, Fei Wang, Litao Ruan

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  15. The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis.International journal of molecular sciences · 2022
    Review
  16. ThymosinCardiovascular therapeutics · 2022
    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

4 authors at 1 institution in 1 country.

Zhen TianDepartment of Ultrasound, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China. tianzhen@xjtufh.edu.cn.ORCID http://orcid.org/0000-0001-7475-9472
Naijuan YaoDepartment of Infectious Diseases, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Fei WangDepartment of Ultrasound, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Litao RuanDepartment of Ultrasound, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation plays a critical role in the progression of pulmonary fibrosis. Thymosin β4 (Tβ4) has antioxidant, anti-inflammatory, and antifibrotic effects. Although the potent protective role of Tβ4 in bleomycin-induced pulmonary fibrosis has been validated, the underlying mechanism is not clear; moreover, the influence of Tβ4 on lipopolysaccharide (LPS)-induced lung injury/fibrosis has not been reported. Expression of Tβ4 in fibrotic lung tissues was assessed by real-time quantitative reverse-transcription PCR (rt-PCR), immunohistochemistry (IHC), and western blotting. The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on LPS-induced lung injury and fibrosis were observed through the evaluation of collagen deposition and α-smooth muscle actin (SMA) expression. In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4. In this study, we evaluated the role of Tβ4 in pulmonary fibrosis and explored the possible underlying mechanisms. Tβ4 was markedly upregulated in human or mouse fibrotic lung tissues. AAV-Tβ4 markedly alleviated LPS-induced oxidative damage, lung injury, inflammation, and fibrosis in mice. Our in vitro experiments also showed that LPS inhibited mitophagy and promoted inflammation via oxidative stress in HPAEpiC, and Tβ4 significantly attenuated LPS-induced mitophagy inhibition, inflammasome activation, and transforming growth factor-β (TGF)-β1-induced epithelial-mesenchymal transition (EMT) in HPAEpiC. Moreover, Tβ4 suppressed the proliferation and attenuated the TGF-β1-induced activation of HLF-1 cells. In conclusion, Tβ4 alleviates LPS-induced lung injury, inflammation, and subsequent fibrosis in mice, suggesting that Tβ4 has a protective role in the pathogenesis of pulmonary fibrosis. Tβ4 is involved in attenuating oxidative injury, promoting mitophagy, and alleviating inflammation and fibrosis. Modulation of Tβ4 might be a novel strategy for treating pulmonary fibrosis.

Indexed as

AnimalsHumansInflammationLipopolysaccharidesMaleMiceMice, Inbred ICRMitophagyOxidative StressPulmonary FibrosisThymosinThymosin beta(4)LipopolysaccharidesThymosinThymosin beta(4)Adeno-associated virusMitophagy.Oxidative stressPulmonary fibrosisThymosin β4

Identifiers

PMID34414534
OpenAlexW3195744366

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.