Evidence map›Paper›PMID 36670464›Full record

ArticleCell & bioscience2023

Hypofucosylation of Unc5b regulated by Fut8 enhances macrophage emigration and prevents atherosclerosis.

Xi Yang, Limei Ma, Jun Zhang, Linmu Chen, Zhen Zou, Di Shen, Hui He, Lei Zhang, Jun Chen, Zhiyi Yuan and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeting Unc5b in macrophages drives atherosclerosis regression and pro-resolving immune cell function.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

12 authors at 2 institutions in 1 country.

Xi Yang *Institute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Limei Ma *College of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Jun ZhangInstitute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Linmu ChenInstitute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Zhen ZouInstitute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Di ShenInstitute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Hui HeInstitute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Lei ZhangCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Jun ChenCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Zhiyi YuanCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Xia QinCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Chao YuCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China. yuchao@cqmu.edu.cn.ORCID http://orcid.org/0000-0002-8391-4080
Chongqing Medical University · CNInner Mongolia Medical University · CN

Funding

Chongqing Foundation and Advanced Research Project CSTC2015jcyjBX0053Chongqing Medical University Scientific Research Cultivating Fund No. 201414Inner Mongolia Medical University PhD Start-up Fund NO.YKD2020BSJJ007National Natural Science Foundation of Chin 81800389Natural Science Foundation of Inner Mongolia No.2020MS08043Natural Science Foundation of Inner Mongolia Autonomous Region No.2021MS08149Natural Science Foundation of the Chongqing Science and Technology Committee cstc2015jcyjA10002
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is the leading underlying cause of the majority of clinical cardiovascular events. Retention of foamy macrophages in plaques is the main factor initiating and promoting the atherosclerotic process. Our previous work showed that ox-LDL induced macrophage retention in plaques and that the guidance receptor Uncoordinated-5 homolog B (Unc5b) was involved in this process. However, little is known about the role of Unc5b in regulating macrophage accumulation within plaques.

resultsIn the present study, we found that Unc5b controls macrophage migration and thus promotes plaque progression in ApoE

conclusionThese results demonstrated that hypofucosylation of Unc5b regulated by Fut8 is positively associated with the delay of the atherosclerotic process by promoting the migration of foamy macrophages. These findings identify a promising therapeutic target for atherosclerosis.

Indexed as

AtherosclerosisFucosylationFut8MacrophagesUnc5b

Identifiers

PMID36670464
PMCPMC9854080
OpenAlexW4317555852

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.