Evidence map›Paper›PMID 27329825›Full record

ArticleScientific reports2016

β-Aminopropionitrile monofumarate induces thoracic aortic dissection in C57BL/6 mice.

Weihong Ren, Yan Liu, Xuerui Wang, Lixin Jia, Chunmei Piao, Feng Lan, Jie Du

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Integrin Signaling Pathways in Aortic Aneurysm and Dissection.Reviews in cardiovascular medicine · 2026
    Review
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  8. Article
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  11. Article
  12. Copy number loss Of APP cause thoracic aortic dissection.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  13. Article
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  15. Review
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  17. Article
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  19. Article
  20. Sex differences and role of lysyl oxidase-like 2 in angiotensin II-induced hypertension in mice.American journal of physiology. Heart and circulatory physiology · 2024
    Article

23 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Weihong RenBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Yan LiuBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Xuerui WangBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Lixin JiaBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Chunmei PiaoBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Feng LanBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Jie DuBeijing Anzhen Hospital, Affiliated to Capital Medical University; Collaborative Innovation Center for Cardiovascular Disorders; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education; Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
Capital Medical University · CNBeijing Anzhen Hospital · CNMinistry of Education · ROSouth China Institute of Collaborative Innovation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thoracic aortic dissection (TAD) is a catastrophic disease with high mortality and morbidity, characterized by fragmentation of elastin and loss of smooth muscle cells. However, the underlying pathological mechanisms of this disease remain elusive because there are no appropriate animal models, limiting discovery of effective therapeutic strategies. We treated mice on C57BL/6 and FVB genetic backgrounds with β-aminopropionitrile monofumarate (BAPN), an irreversible inhibitor of lysyl oxidase, for 4 wk, followed by angiotensin II (Ang II) infusion for 24 h. We found that the BAPN plus Ang II treatment induced formation of aortic dissections in 100% of mice on both genetic backgrounds. BAPN without Ang II caused dissections in few FVB mice, but caused 87% of C57BL/6 mice to develop TAD, with 37% dying from rupture of the aortic dissection. Moreover, a lower dose of BAPN induced TAD formation and rupture earlier with fewer effects on body weight. Therefore, we have generated a reliable and convenient TAD model in C57BL/6 mice for studying the pathological process and exploring therapeutic targets of TAD.

Indexed as

ActinsAminopropionitrileAngiotensin IIAnimalsAortic Aneurysm, ThoracicBlood PressureBody WeightCollagen Type ICollagen Type I, alpha 1 ChainDisease Models, AnimalHumansMatrix Metalloproteinase 9MiceMice, Inbred C57BLMyosin Heavy ChainsPhenotypeActinsalpha-smooth muscle actin, mouseAminopropionitrileAngiotensin IICollagen Type ICollagen Type I, alpha 1 ChainMatrix Metalloproteinase 9Myosin Heavy Chains

Identifiers

PMID27329825
PMCPMC4916438
OpenAlexW2465125755

What OpenQuestion holds

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LicenceCC BY
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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.