Evidence map›Paper›PMID 35477975›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2022

Exosomes derived from hypoxia-induced alveolar epithelial cells stimulate interstitial pulmonary fibrosis through a HOTAIRM1-dependent mechanism.

Lin Chen, Yang Yang, Ruiming Yue, Xiaying Peng, Hua Yu, XiaoBo Huang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Immune Mechanisms of Pulmonary Fibrosis with Bleomycin.International journal of molecular sciences · 2023
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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

6 authors at 1 institution in 1 country.

Lin ChenDepartment of Respiratory and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, P. R. China.
Yang YangDepartment of Respiratory and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, P. R. China.
Ruiming YueChinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, P. R. China.
Xiaying PengDepartment of Respiratory and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, P. R. China.
Hua YuChinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, P. R. China.
XiaoBo HuangChinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, P. R. China. huangxiaobo@med.uestc.edu.cn.ORCID 0000-0002-9265-5279
University of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is the result of various diseases with no satisfactory treatment approaches. The exosome-mediated transfer of long noncoding RNAs (lncRNAs) has been implicated in the pathological process of lung diseases. Herein, we investigated the therapeutic potential of HOTAIRM1 transferred by alveolar epithelial cell (AEC)-derived exosomes in interstitial pulmonary fibrosis (IPF) and the potential molecular mechanisms. Next-generation sequencing-based gene expression profiling was employed to identify lncRNAs related to IPF. Exosomes were isolated from hypoxia-induced AECs (AEC-exosomes) and identified before use. HOTAIRM1 expression was examined in bleomycin-induced IPF mouse models and the isolated exosomes, and the miRNA downstream of HOTAIRM1 was analyzed. HOTAIRM1 expression was increased in the lung tissues of IPF mice and AEC exosomes. HOTAIRM1 delivered by AEC-exosomes promoted the proliferation and transdifferentiation of lung fibroblasts (LFs). Mechanistically, HOTAIRM1 competitively bound to miR-30d-3p and recruited YY1 to upregulate HSF1 expression. In addition, miR-30d-3p targeted HSF1 by binding to its 3'-UTR and reduced its expression. In vivo assays confirmed the promoting effect of exosomes-HOTAIRM1 on extracellular matrix remodeling by regulating the miR-30d-3p/HSF1/YY1 axis. Overall, HOTAIRM1 loaded by AEC exosomes can accelerate IPF by disrupting miR-30d-3p-mediated inhibition of HSF1 and inducing recruitment of HSF1 by YY1. These results highlight a promising strategy to overcome IPF.

Indexed as

ExosomesIdiopathic Pulmonary FibrosisMicroRNAsRNA, Long Noncoding3' Untranslated RegionsAlveolar Epithelial CellsAnimalsCell ProliferationHypoxiaMice3' Untranslated RegionsHOTAIR long non-coding RNA, mouseMicroRNAsRNA, Long Noncoding

Identifiers

PMID35477975
OpenAlexW4225101414

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.