Evidence map›Paper›PMID 23263331›Full record

ArticleCardiovascular research2013

Interleukin-17 causes Rho-kinase-mediated endothelial dysfunction and hypertension.

Hoanglan Nguyen, Valorie L Chiasson, Piyali Chatterjee, Shelley E Kopriva, Kristina J Young, Brett M Mitchell

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 3 pooled it
4.5field-weighted citation impact, top 5% 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

179 citing papers in PubMed, 3 syntheses or guidelines pooled it, 301 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  18. Article
  19. Review
  20. Identification of potential biomarkers for hypertension based on transcriptomic analysis in rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article

119 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

6 authors at 2 institutions in 1 country.

Hoanglan NguyenDivision of Nephrology & Hypertension, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine/Scott & White Memorial Hospital, 702 SW HK Dodgen Loop, Temple, TX 76504, USA.
Valorie L Chiasson
Piyali Chatterjee
Shelley E Kopriva
Kristina J Young
Brett M Mitchell
Scott & White Memorial Hospital · USTexas A&M Health Science Center · US

Funding

Role of FKBP12/12.6 in Endothelial FunctionR01HL084299 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MITCHELL, BRETT M · 2007 to 2011
$1.3M
Role of Immune Cells in Immunosuppressive Drug-Induced HypertensionR56HL084299 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MITCHELL, BRETT M · 2013 to 2013
$364k
NHLBI NIH HHS HL084299NHLBI NIH HHS R01 HL084299NHLBI NIH HHS R56 HL084299
6 · The paper itself

Abstract

aimsElevated levels of pro-inflammatory cytokine interleukin-17A (IL-17) are associated with hypertensive autoimmune diseases; however, the connection between IL-17 and hypertension is unknown. We hypothesized that IL-17 increases blood pressure by decreasing endothelial nitric oxide production. METHODS AND

resultsAcute treatment of endothelial cells with IL-17 caused a significant increase in phosphorylation of the inhibitory endothelial nitric oxide (NO) synthase residue threonine 495 (eNOS Thr495). Of the kinases known to phosphorylate eNOS Thr495, only inhibition of Rho-kinase prevented the IL-17-induced increase. IL-17 caused a threefold increase in the Rho-kinase activator RhoA, and this was prevented by an IL-17 neutralizing antibody. In isolated mouse aortas, IL-17 significantly increased eNOS Thr495 phosphorylation, induced RhoA expression, and decreased NO-dependent relaxation responses, all of which were prevented by either an IL-17 neutralizing antibody or inhibition of Rho-kinase. In mice, IL-17 treatment for 1 week significantly increased systolic blood pressure and this was associated with decreased aortic NO-dependent relaxation responses, increased eNOS Thr495 phosphorylation, and increased RhoA expression. Inhibition of Rho-kinase prevented the hypertension caused by IL-17.

conclusionThese data demonstrate that IL-17 activates RhoA/Rho-kinase leading to endothelial dysfunction and hypertension. Inhibitors of IL-17 or Rho-kinase may prove useful as anti-hypertensive drugs in IL-17-associated autoimmune diseases.

Indexed as

AmidesAnimalsEndothelial CellsHypertensionInterleukin-17MaleMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIPhosphorylationPyridinesRatsrho-Associated KinasesAmidesInterleukin-17Nitric OxideNitric Oxide Synthase Type IIIPyridinesrho-Associated KinasesY 27632

Identifiers

PMID23263331
PMCPMC3583258
OpenAlexW2167750356

What OpenQuestion holds

Textmetadata
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.