Evidence map›Paper›PMID 36291750›Full record

ArticleBiomolecules2022

Type I Interferon Receptor Subunit 1 Deletion Attenuates Experimental Abdominal Aortic Aneurysm Formation.

Takahiro Shoji, Jia Guo, Yingbin Ge, Yankui Li, Gang Li, Toru Ikezoe, Wei Wang, Xiaoya Zheng, Sihai Zhao, Naoki Fujimura and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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 5 institutions in 3 countries.

Takahiro ShojiDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0003-2945-8421
Jia GuoDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-4574-4543
Yingbin GeDepartment of Physiology, Nanjing Medical University, Nanjing 210093, China.ORCID 0000-0003-1471-9000
Yankui LiDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gang LiDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Toru IkezoeDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Wei WangDepartment of Vascular Surgery, Central South University Xiangya Hospital, Changsha 410008, China.
Xiaoya ZhengDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Sihai ZhaoDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-5845-6639
Naoki FujimuraDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-8714-7723
Jianhua HuangDepartment of Vascular Surgery, Central South University Xiangya Hospital, Changsha 410008, China.
Baohui XuDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-2857-7464
Ronald L DalmanDepartment of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Stanford University · USCentral South University · CNNanjing Medical University · CNSaiseikai Central Hospital · JPShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveType I interferon receptor signaling contributes to several autoimmune and vascular diseases such as lupus, atherosclerosis and stroke. The purpose of this study was to assess the influence of type I interferon receptor deficiency on the formation and progression of experimental abdominal aortic aneurysms (AAAs).

methodsAAAs were induced in type I interferon receptor subunit 1 (IFNAR1)-deficient and wild type control male mice via intra-infrarenal aortic infusion of porcine pancreatic elastase. Immunostaining for IFNAR1 was evaluated in experimental and clinical aneurysmal abdominal aortae. The initiation and progression of experimental AAAs were assessed via ultrasound imaging prior to (day 0) and days 3, 7 and 14 following elastase infusion. Aneurysmal histopathology was analyzed at sacrifice.

resultsIncreased aortic medial and adventitial IFNAR1 expression was present in both clinical AAAs harvested at surgery and experimental AAAs. Following AAA induction, wild type mice experienced progressive, time-dependent infrarenal aortic enlargement. This progression was substantially attenuated in IFNAR1-deficient mice. On histological analyses, medial elastin degradation, smooth muscle cell depletion, leukocyte accumulation and neoangiogenesis were markedly diminished in IFNAR1-deficient mice in comparison to wild type mice.

conclusionIFNAR1 deficiency limited experimental AAA progression in response to intra-aortic elastase infusion. Combined with clinical observations, these results suggest an important role for IFNAR1 activity in AAA pathogenesis.

Indexed as

Aortic Aneurysm, AbdominalAnimalsDisease Models, AnimalElastinMaleMiceMice, Inbred C57BLPancreatic ElastaseReceptor, Interferon alpha-betaSwineElastinPancreatic ElastaseReceptor, Interferon alpha-betaabdominal aortic aneurysmangiogenesisleukocytestype I interferon receptor

Identifiers

PMID36291750
PMCPMC9599283
OpenAlexW4307271541

What OpenQuestion holds

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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.