Evidence map›Paper›PMID 34459250›Full record

ArticleJournal of the American Heart Association2021

Recombinant Interleukin-19 Suppresses the Formation and Progression of Experimental Abdominal Aortic Aneurysms.

Hiroki Tanaka, Baohui Xu, Haojun Xuan, Yingbin Ge, Yan Wang, Yankui Li, Wei Wang, Jia Guo, Sihai Zhao, Keith J Glover and 12 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

22 authors at 6 institutions in 3 countries.

Hiroki TanakaDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Baohui XuDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.ORCID 0000-0002-2857-7464
Haojun XuanDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Yingbin GeDepartment of Physiology Nanjing Medical University Nanjing Jiangsu China.ORCID 0000-0003-1471-9000
Yan WangPeking University Third HospitalMedical Research Center Haidian Beijing China.
Yankui LiDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.ORCID 0000-0001-8048-0910
Wei WangDepartment of Surgery Xiangya HospitalSouth Central University School of Medicine Changsha Hunan China.ORCID 0000-0002-0957-5762
Jia GuoDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Sihai ZhaoDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Keith J GloverDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Xiaoya ZhengDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Shuai LiuDepartment of Surgery Xiangya HospitalSouth Central University School of Medicine Changsha Hunan China.
Kazunori InuzukaDivision of Vascular Surgery Hamamatsu University School of Medicine Hamamatsu Shizuoka Japan.
Naoki FujimuraDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Yuko FurushoDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.ORCID 0000-0003-3823-5166
Toru IkezoeDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Takahiro ShojiDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.ORCID 0000-0003-2945-8421
Lixin WangDepartment of Vascular Surgery Zhongshan HospitalFudan University Shanghai China.
Weiguo FuDepartment of Vascular Surgery Zhongshan HospitalFudan University Shanghai China.
Jianhua HuangDepartment of Surgery Xiangya HospitalSouth Central University School of Medicine Changsha Hunan China.
Naoki UnnoDivision of Vascular Surgery Hamamatsu University School of Medicine Hamamatsu Shizuoka Japan.
Ronald L DalmanDivison of Vascular Surgery Department of Surgery Stanford University School of Medicine Stanford CA.
Stanford University · USCentral South University · CNHamamatsu University School of Medicine · JPFudan University · CNNanjing Medical University · CNPeking University · CN

Funding

Critical Role of Inflammatory Macrophages in AAA PathogenesisR21HL109750 · NHLBI · STANFORD UNIVERSITY · PI DALMAN, RONALD L · 2011 to 2012
$437k
Mechanisms and Significance of Angiogenesis in AAA DiseaseR21HL112122 · NHLBI · STANFORD UNIVERSITY · PI DALMAN, RONALD L · 2012 to 2013
$423k
NHLBI NIH HHS R21 HL109750NHLBI NIH HHS R21 HL112122
6 · The paper itself

Abstract

Background Interleukin-19 is an immunosuppressive cytokine produced by immune and nonimmune cells, but its role in abdominal aortic aneurysm (AAA) pathogenesis is not known. This study aimed to investigate interleukin-19 expression in, and influences on, the formation and progression of experimental AAAs. Methods and Results Human specimens were obtained at aneurysm repair surgery or from transplant donors. Experimental AAAs were created in 10- to 12-week-old male mice via intra-aortic elastase infusion. Influence and potential mechanisms of interleukin-19 treatment on AAAs were assessed via ultrasonography, histopathology, flow cytometry, and gene expression profiling. Immunohistochemistry revealed augmented interleukin-19 expression in both human and experimental AAAs. In mice, interleukin-19 treatment before AAA initiation via elastase infusion suppressed aneurysm formation and progression, with attenuation of medial elastin degradation, smooth-muscle depletion, leukocyte infiltration, neoangiogenesis, and matrix metalloproteinase 2 and 9 expression. Initiation of interleukin-19 treatment after AAA creation limited further aneurysmal degeneration. In additional experiments, interleukin-19 treatment inhibited murine macrophage recruitment following intraperitoneal thioglycolate injection. In classically or alternatively activated macrophages in vitro, interleukin-19 downregulated mRNA expression of inducible nitric oxide synthase, chemokine C-C motif ligand 2, and metalloproteinases 2 and 9 without apparent effect on cytokine-expressing helper or cytotoxic T-cell differentiation, nor regulatory T cellularity, in the aneurysmal aorta or spleen of interleukin-19-treated mice. Interleukin-19 also suppressed AAAs created via angiotensin II infusion in hyperlipidemic mice. Conclusions Based on human evidence and experimental modeling observations, interleukin-19 may influence the development and progression of AAAs.

Indexed as

Aortic Aneurysm, AbdominalAnimalsCytokinesDisease Models, AnimalInterleukinsMaleMatrix Metalloproteinase 2MiceMice, Inbred C57BLPancreatic ElastaseRecombinant ProteinsCytokinesInterleukinsMatrix Metalloproteinase 2Pancreatic ElastaseRecombinant Proteinsabdominal aortic aneurysmangiogenesiscytokinesinterleukin‐19macrophages

Identifiers

PMID34459250
PMCPMC8649236
OpenAlexW3197705344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.