Evidence map›Paper›PMID 33101872›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

E3 Ligase FBXW2 Is a New Therapeutic Target in Obesity and Atherosclerosis.

Cheng Wang, Wenjing Xu, Yuelin Chao, Minglu Liang, Fengxiao Zhang, Kai Huang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. TRIM56 Promotes White Adipose Tissue Browning to Attenuate Obesity by Degrading TLE3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Review
  7. Ubiquitination and Metabolic Disease.Advances in experimental medicine and biology · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. E3 Ligase FBXW2 Is a New Therapeutic Target in Obesity and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    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

6 authors at 2 institutions in 1 country.

Cheng WangClinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.ORCID https://orcid.org/0000-0001-7185-2671
Wenjing XuClinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Yuelin ChaoDepartment of Cardiology Nanjing First Hospital Nanjing Medical University Nanjing 210029 China.
Minglu LiangClinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Fengxiao ZhangClinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Kai HuangClinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China.
Union Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic low-grade inflammation orchestrated by macrophages plays a critical role in metabolic chronic diseases, like obesity and atherosclerosis. However, the underlying mechanism remains to be elucidated. Here, the E3 ubiquitin ligase F-box/WD Repeat-Containing Protein 2 (FBXW2), the substrate-binding subunit of E3 ubiquitin ligase SCF (a complex of FBXW2, SKP1, and cullin-1), as an inflammatory mediator in macrophages, is identified. Myeloid-specific FBXW2 gene deficiency improves both obesity-associated with insulin resistance and atherosclerosis in murine models. The beneficial effects by FBXW2 knockout are accompanied by decreased proinflammatory responses and macrophage infiltration in the microenvironment. Mechanistically, it is identified that KH-type splicing regulatory protein (KSRP) is a new bona fide ubiquitin substrate of SCF

Indexed as

atherosclerosisFBXW2inflammationinsulin resistanceKSRPobesity

Identifiers

PMID33101872
PMCPMC7578860
OpenAlexW3081846112

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.