Evidence mapPaperPMID 34716308Full record

ArticleCell death & disease2021

Chromatin accessibility analysis identifies the transcription factor ETV5 as a suppressor of adipose tissue macrophage activation in obesity.

Ren-Dong Hu, Wen Zhang, Liang Li, Zu-Qi Zuo, Min Ma, Jin-Fen Ma, Ting-Ting Yin, Cai-Yue Gao, Shu-Han Yang, Zhi-Bin Zhao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024
    Review
  8. Article
  9. 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

14 authors at 5 institutions in 2 countries.

Ren-Dong Hu *Chronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Wen Zhang *Institute of Artificial Intelligence, Hefei Comprehensive National Science Center, Hefei, Anhui, China.
Liang LiGuangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China. lil2009@scut.edu.cn.ORCID 0000-0003-0745-2571
Zu-Qi ZuoInstitute of Artificial Intelligence, Hefei Comprehensive National Science Center, Hefei, Anhui, China.
Min MaChronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Jin-Fen MaChronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Ting-Ting YinDepartment of General Surgery, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, Guangdong, China.
Cai-Yue GaoChronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Shu-Han YangChronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Zhi-Bin ZhaoGuangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.
Zi-Jun LiGuangdong Provincial Institute of Geriatrics, Concord Medical Center, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.ORCID 0000-0002-3029-5001
Gui-Bin QiaoDepartment of Thoracic Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.
Zhe-Xiong LianChronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China. zxlian@scut.edu.cn.ORCID 0000-0002-9525-1421
Kun QuInstitute of Artificial Intelligence, Hefei Comprehensive National Science Center, Hefei, Anhui, China. qukun@ustc.edu.cn.ORCID 0000-0002-5555-8437
South China University of Technology · CNGuangdong Academy of Medical Sciences · CNGuangzhou First People's Hospital · CNGuangzhou Regenerative Medicine and Health Guangdong Laboratory · CNNational Science Centre · PL

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31771428National Natural Science Foundation of China (National Science Foundation of China) 31970858National Natural Science Foundation of China (National Science Foundation of China) 81801607National Natural Science Foundation of China (National Science Foundation of China) 91940306
6 · The paper itself

Abstract

Activation of adipose tissue macrophages (ATMs) contributes to chronic inflammation and insulin resistance in obesity. However, the transcriptional regulatory machinery involved in ATM activation during the development of obesity is not fully understood. Here, we profiled the chromatin accessibility of blood monocytes and ATMs from obese and lean mice using assay for transposase-accessible chromatin sequencing (ATAC-seq). We found that monocytes and ATMs from obese and lean mice exhibited distinct chromatin accessibility status. There are distinct regulatory elements that are specifically associated with monocyte or ATM activation in obesity. We also discovered several transcription factors that may regulate monocyte and ATM activation in obese mice, specifically a predicted transcription factor named ETS translocation variant 5 (ETV5). The expression of ETV5 was significantly decreased in ATMs from obese mice and its downregulation was mediated by palmitate stimulation. The decrease in ETV5 expression resulted in macrophage activation. Our results also indicate that ETV5 suppresses endoplasmic reticulum (ER) stress and Il6 expression in macrophages. Our work delineates the changes in chromatin accessibility in monocytes and ATMs during obesity, and identifies ETV5 as a critical transcription factor suppressing ATM activation, suggesting its potential use as a therapeutic target in obesity-related chronic inflammation.

Indexed as

Adipose TissueAnimalsChromatinDiet, High-FatDisease Models, AnimalDNA-Binding ProteinsHEK293 CellsHumansInflammationInsulin ResistanceMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BLMonocytesChromatinDNA-Binding ProteinsETV5 protein, humanEtv5 protein, mouseTranscription Factors

Identifiers

PMID34716308
PMCPMC8556336
OpenAlexW3208710497

What Socratic 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 Socratic graph.