Evidence map›Paper›PMID 34936241›Full record

ArticleClinical and translational medicine2021

A reduction in the vascular smooth muscle cell focal adhesion component syndecan-4 is associated with abdominal aortic aneurysm formation.

Jiaxin Hu, Yuyu Li, Zhonghai Wei, Haiting Chen, Xuan Sun, Qing Zhou, Qi Zhang, Yong Yin, Meng Guo, Jianzhou Chen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Role of miR-21-5p in the pathogenesis of abdominal aortic aneurysm regarding the Th17 pathway.International journal of cardiology. Heart & vasculature · 2025
    Article
  3. Review
  4. Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

13 authors at 2 institutions in 1 country.

Jiaxin HuDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Yuyu LiDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Zhonghai WeiDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Haiting ChenDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Xuan SunDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Qing ZhouDepartment of Cardiac Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, China.
Qi ZhangDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Yong YinDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Meng GuoDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Jianzhou ChenDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Guangyao ZhaiDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Biao XuDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Jun XieDepartment of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.ORCID 0000-0002-9385-3242
Nanjing Drum Tower Hospital · CNCapital Medical University · CN

Funding

The Fundamental Research Funds for the Central Universities 14380501/0214The Key Projects of Science and Technology of Jiangsu Province BE2019602The Natural Science Foundation of China 81700389The Natural Science Foundation of China 81700392The Natural Science Foundation of China 81870358The Natural Science Foundation of China 92068116The Science Fund for Distinguished Young Scholars in Jiangsu Province BK20211501
6 · The paper itself

Abstract

backgroundAbdominal aortic aneurysm (AAA) is a serious vascular disease for which there is no effective drug treatment. The incidence of AAA increases significantly as a subject ages, and the molecular mechanism of AAA formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), an important component of focal adhesions, in AAA formation and its association with phenotypic changes in vascular smooth muscle cells (VSMCs). METHODS AND

resultsThe protein expression levels of SDC4 were significantly decreased in human AAA tissue and those of an AAA mouse model. Moreover, SDC4 knockout (KO) in mice accelerated the formation and rupture of AAAs induced by angiotensin II (Ang II) and calcium chloride (CaCl

conclusionWe herein demonstrated that silencing SDC4 was associated with increased AAA formation and phenotypic changes in VSMCs via the RhoA-F/G-actin-MRTF-A pathway. These findings indicated that a reduction in SDC4 expression was an important pathological alteration and potential therapeutic target for AAA formation.

Indexed as

Analysis of VarianceAnimalsAortic Aneurysm, AbdominalChinaDisease Models, AnimalFocal AdhesionsMiceMice, Inbred C57BLMuscle, Smooth, VascularSyndecan-4SDC4 protein, humanSyndecan-4abdominal aortic aneurysmF/G-actin-MRTF-Aphenotypic changeRhoAsyndecan-4

Identifiers

PMID34936241
PMCPMC8693440
OpenAlexW4200370569

What OpenQuestion holds

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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.