Evidence map›Paper›PMID 29514135›Full record

ArticleAging2018

CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function.

Lu Han, Lu Dai, Yuan-Fei Zhao, Hai-Yang Li, Ou Liu, Feng Lan, Wen-Jian Jiang, Hong-Jia Zhang

Erratum issuedOpen access · greenAbstract readHistorical Article
In one paragraph

Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  12. The Role of Macrophages in Aortic Dissection.Frontiers in physiology · 2020
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Lu Han *Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Lu Dai *Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yuan-Fei Zhao *Centre for Transplant and Renal Research, The Westmead Institute for Medical Research, University of Sydney, Sydney, Australia.
Hai-Yang LiDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Ou LiuDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Feng LanDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Wen-Jian JiangDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Hong-Jia ZhangDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Beijing Institute of Water · CNBeijing Anzhen Hospital · CNCapital Medical University · CNUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute aortic dissection is one of the most lethal cardiovascular disease. The major histopathological feature of AAD is medial degradation, especially breakdown of elastin and collagen. However, the underlying mechanism remains a mystery. Platelets expressed CD40 Ligand (CD40L) is recently recognised as a key effector of cardiovascular disease development through its pro-inflammatory effect. To clarify the role of CD40L in AAD, we examined level of CD40L in human blood serum samples and found that it is significantly higher in AAD patients compared with healthy subjects (26.8±5.52 ng/mL versus 13.4±4.00 ng/mL). To further investigate if CD40L is involve in the development of AAD, we applied β-aminopropionitrile (BAPN) induced mouse model of AAD. Consistent with the human data, circulating CD40L in AAD mice much higher than normal mice (148.40±75.96 pg/mL versus 44.09±19.65 pg/mL). Meanwhile, multiple pro-inflammatory chemokines significantly increased in AAD mice. Importantly, the CD40L-/- mice treated with BAPN did not develop these phenotypes. Lastly, we confirmed that endothelial cells migration was significantly inhibited by CD40L, suggesting impaired recovery from intimal injury. In summary, we found that CD40L promoted AAD development through its pro-inflammatory effects and inhibition of endothelial cell function.

Indexed as

AminopropionitrileAnimalsAortic DissectionBlood PlateletsCase-Control StudiesCD40 LigandEndothelial CellsFemaleGene Expression RegulationHistory, 16th CenturyHistory, 17th CenturyHistory, 18th CenturyHumansInflammationMaleMiceAminopropionitrileCD40 Ligandacute aortic dissectionCD40Lendothelial cell

Identifiers

PMID29514135
PMCPMC5892687
OpenAlexW2790781434

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.