Evidence map›Paper›PMID 29853563›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2018

Deficiency of FAM3D (Family With Sequence Similarity 3, Member D), A Novel Chemokine, Attenuates Neutrophil Recruitment and Ameliorates Abdominal Aortic Aneurysm Development.

Li He, Yi Fu, Jingna Deng, Yicong Shen, Yingbao Wang, Fang Yu, Nan Xie, Zhongjiang Chen, Tianpei Hong, Xinjian Peng and 6 more

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Integrin Signaling Pathways in Aortic Aneurysm and Dissection.Reviews in cardiovascular medicine · 2026
    Review
  3. The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. The mechanism and therapy of aortic aneurysms.Signal transduction and targeted therapy · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Computational and mathematical methods in medicine · 2022
    Article
  18. Review
  19. Article
  20. 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

16 authors at 3 institutions in 1 country.

Li HeFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Yi FuFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Jingna DengTasly Microcirculation Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China (J.D., J.H.).
Yicong ShenFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Yingbao WangFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Fang YuFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Nan XieFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Zhongjiang ChenFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Tianpei HongDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, People's Republic of China (T.H.).
Xinjian PengDepartment of Immunology, School of Basic Medical Sciences, and Key Laboratory of Medical Immunology of Ministry of Health, Peking University Health Science Center, Beijing, People's Republic of China (X.P., Q.L., Ying Wang).
Qingqing LiDepartment of Immunology, School of Basic Medical Sciences, and Key Laboratory of Medical Immunology of Ministry of Health, Peking University Health Science Center, Beijing, People's Republic of China (X.P., Q.L., Ying Wang).
Jing ZhouFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.).
Jingyan HanTasly Microcirculation Research Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China (J.D., J.H.) kongw@bjmu.edu.cn jzxi@pku.edu.cn yw@bjmu.edu.cn hanjingyan@bjmu.edu.cn.
Ying WangDepartment of Immunology, School of Basic Medical Sciences, and Key Laboratory of Medical Immunology of Ministry of Health, Peking University Health Science Center, Beijing, People's Republic of China (X.P., Q.L., Ying Wang) kongw@bjmu.edu.cn jzxi@pku.edu.cn yw@bjmu.edu.cn hanjingyan@bjmu.edu.cn.
Jianzhong XiDepartment of Biomedicine, College of Engineering, Peking University, Beijing, People's Republic of China (J.X.). kongw@bjmu.edu.cn jzxi@pku.edu.cn yw@bjmu.edu.cn hanjingyan@bjmu.edu.cn.
Wei KongFrom the Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, People's Republic of China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, People's Republic of China (L.H., Y.F., Y.S., Yingbao Wang., F.Y., N.X., Z.C., J.Z., W.K.) kongw@bjmu.edu.cn jzxi@pku.edu.cn yw@bjmu.edu.cn hanjingyan@bjmu.edu.cn.
Peking University · CNMinistry of Education of the People's Republic of China · CNPeking University Third Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChemokine-mediated neutrophil recruitment contributes to the pathogenesis of abdominal aortic aneurysm (AAA) and may serve as a promising therapeutic target. FAM3D (family with sequence similarity 3, member D) is a recently identified novel chemokine. Here, we aimed to explore the role of FAM3D in neutrophil recruitment and AAA development. APPROACH AND

resultsFAM3D was markedly upregulated in human AAA tissues, as well as both elastase- and CaPO

conclusionsFAM3D, as a dual agonist of FPR1 and FPR2, induced Mac-1-mediated neutrophil recruitment and aggravated AAA development through FPR-related Gi protein and β-arrestin signaling.

Indexed as

Neutrophil InfiltrationAnimalsAorta, AbdominalAortic Aneurysm, Abdominalbeta-ArrestinsCells, CulturedCoculture TechniquesCytokinesDisease Models, AnimalHumansLeukocyte RollingMacrophage-1 AntigenMaleMice, Inbred C57BLMice, Knockout, ApoENeutrophilsbeta-ArrestinsCytokinesFAM3D protein, humanFAM3D protein, mouseformyl peptide receptor 2, mouseFpr1 protein, mouseMacrophage-1 AntigenReceptors, Formyl Peptideabdominal aortic aneurysmchemokineendothelial cellG protein coupled receptorneutrophil recruitment

Identifiers

PMID29853563
PMCPMC6039426
OpenAlexW2807535153

What Socratic 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 Socratic graph.