Evidence map›Paper›PMID 39323641›Full record

ArticleFrontiers in pharmacology2024

Triiodothyronine acts on DAO to regulate pulmonary fibrosis progression by facilitating cell senescence through the p53/p21 signaling pathway.

Xiaoshu Guo, Kai Xu, Lan Wang, Linke Ding, Wenwen Li, Xinsheng Zhang, Weiming Zhao, Ningdan Wang, Gaiping Wang, Wenyu Zhao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

12 authors.

Xiaoshu Guo *State Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Kai Xu *State Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Lan WangState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Linke DingState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Wenwen LiState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Xinsheng ZhangState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Weiming ZhaoState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Ningdan WangState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Gaiping WangState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Wenyu ZhaoState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.
Ivan RosasDivision of Pulmonary, Critical Care and Sleep Medicine, Baylor College of Medicine, Houston, TX, United States.
Guoying YuState Key Laboratory Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is the result of multiple cycles of epithelial cell injury and fibroblast activation; currently, there is no clear etiology. Increasing evidence suggests that protein metabolism and amino acids play a crucial role in IPF, but the role of D-amino acids is not yet clear. The aim of this study was to identify novel mediators in order to test the hypothesis that D-amino acid oxidase (DAO) plays a significant role in the pathogenesis of IPF. Methods: We analyzed DAO gene expression in patients with IPF and mice with bleomycin (BLM)-induced lung fibrosis. We performed Results: DAO expression was downregulated in the lungs of IPF patients and BLM-induced fibrotic mice. Treatment with D-serine (D-Ser) or drug inhibition of DAO promoted cell senescence through the p53/p21 pathway. Conclusion: We concluded that the DAO-p53/p21 axis might be a key anti-fibrotic pathway regulating the progress of fibrosis and facilitating the therapeutic role of T

Indexed as

anti-fibrotic axisD-amino acid oxidaseidiopathic pulmonary fibrosisp53/p21 pathwaytriiodothyronine

Identifiers

PMID39323641
PMCPMC11422212

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.