Evidence map›Paper›PMID 28974499›Full record

ArticleJournal of the American Heart Association2017

Interleukin 22 Promotes Blood Pressure Elevation and Endothelial Dysfunction in Angiotensin II-Treated Mice.

Jing Ye, Qingwei Ji, Jianfang Liu, Ling Liu, Ying Huang, Ying Shi, Lei Shi, Menglong Wang, Mengling Liu, Ying Feng and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. Role of Inflammatory and Proresolving Mediators in Endothelial Dysfunction.Basic & clinical pharmacology & toxicology · 2025
    Review
  4. Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022
    Review
  12. Review
  13. Review
  14. NLRP3 inflammasome: The rising star in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Interleukin-22: a potential therapeutic target in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2021
    Review
  19. Article
  20. Immunity and Hypertension.Acta physiologica (Oxford, England) · 2021
    Review
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

16 authors at 4 institutions in 1 country.

Jing YeDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Qingwei JiDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Jianfang LiuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Ling LiuDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Ying HuangDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Ying ShiDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Lei ShiDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Menglong WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Mengling LiuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Ying FengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Huimin JiangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Yao XuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Zhen WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Junlong SongDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Yingzhong LinDepartment of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China yingzhonglin@126.com wanjun1963@126.com.
Jun WanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China yingzhonglin@126.com wanjun1963@126.com.
Wuhan University · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CNRenmin Hospital of Wuhan University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD4+ T helper (Th) cells, including Th1, Th2, and Th17 cells, play critical roles in angiotensin II-induced hypertension. Th22 cells, a novel subset of Th cells, take part in cardiovascular diseases by producing IL-22 (interleukin 22). This study aimed to investigate whether IL-22 is involved in hypertension. METHODS AND

resultsTh22 cells and IL-22 levels were detected in angiotensin II-infused mice, and the results showed that Th22 cells and IL-22 levels significantly increased. To determine the effect of Th22/IL-22 on blood pressure regulation, angiotensin II-infused mice were treated with recombinant mouse IL-22, an anti-IL-22 neutralizing monoclonal antibody, or control. Treatment with recombinant IL-22 resulted in increased blood pressure, amplified inflammatory responses, and aggravated endothelial dysfunction, whereas the anti-IL-22 neutralizing monoclonal antibody decreased blood pressure, reduced inflammatory responses, and attenuated endothelial dysfunction. To determine whether the STAT3 (signal transducer and activator of transcription 3) pathway mediates the effect of IL-22 on blood pressure regulation, the special STAT3 pathway inhibitor S31-201 was administered to mice treated with recombinant IL-22. S31-201 treatment significantly ameliorated the IL-22 effects of increased blood pressure and endothelial dysfunction. In addition, serum IL-22 levels were significantly increased in hypertensive patients compared with healthy persons. Correlation analysis showed a positive correlation between IL-22 levels and blood pressure.

conclusionsIL-22 amplifies the inflammatory response, induces endothelial dysfunction and promotes blood pressure elevation in angiotensin II-induced hypertensive mice. The STAT3 pathway mediates the effect of IL-22 on hypertension. Blocking IL-22 may be a novel therapeutic strategy to prevent and treat hypertension.

Indexed as

Angiotensin IIAdultAgedAnimalsAntibodies, MonoclonalBlood PressureDisease Models, AnimalDose-Response Relationship, DrugEndothelium, VascularFemaleHumansHypertensionInflammation MediatorsInterleukin-22InterleukinsMaleAngiotensin IIAntibodies, MonoclonalInflammation MediatorsInterleukin-22InterleukinsNitric Oxide Synthase Type IIINos3 protein, mouseRecombinant ProteinsStat3 protein, mouseSTAT3 Transcription FactorVasodilator Agentsangiotensin IIendothelial dysfunctionhypertensioninflammationinterleukin

Identifiers

PMID28974499
PMCPMC5721831
OpenAlexW2761179950

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.