Evidence map›Paper›PMID 28280792›Full record

ArticleJACC. Basic to translational science2016

Inhibition of Interleukin 17-A but not Interleukin-17F Signaling Lowers Blood Pressure and Reduces End-organ Inflammation in Angiotensin II-induced Hypertension.

Mohamed A Saleh, Allison E Norlander, Meena S Madhur

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
8.5field-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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Immune and Metabolic Mechanisms of Endothelial Dysfunction.International journal of molecular sciences · 2024
    Review
  15. Immune Mechanisms in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024
    Review
  16. Review
  17. Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024
    Review
  18. Article
  19. Review
  20. Immune cells and hypertension.Immunologic research · 2024
    Review

20 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

3 authors at 3 institutions in 2 countries.

Mohamed A SalehDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.
Allison E NorlanderDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville TN, USA.
Meena S MadhurDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville TN, USA.
Mansoura University · EGVanderbilt University · USVanderbilt University Medical Center · US

Funding

Immunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5M
Diverse Roles of Interleukin 17 Isoforms in the Pathogenesis of HypertensionK08HL121671 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MADHUR, MEENAKSHI SWAMINATHAN · 2014 to 2018
$723k
The Effect of Salt on T Cell Function in HypertensionF31HL127986 · NHLBI · VANDERBILT UNIVERSITY · PI NORLANDER, ALLISON ELIZABETH · 2015 to 2016
$46k
NHLBI NIH HHS F31 HL127986NHLBI NIH HHS K08 HL121671NHLBI NIH HHS T32 HL069765
6 · The paper itself

Abstract

objectivesTo characterize the T cell subsets producing interleukin 17 (IL-17) isoforms A and F in hypertensive kidneys and vessels and determine whether inhibition of IL-17 signaling lowers blood pressure and end-organ damage in a mouse model of hypertension.

backgroundT cell derived cytokines play a central role in the pathophysiology of hypertension and contribute to end-organ dysfunction. We previously showed that mice genetically deficient in IL-17A exhibited blunted hypertension and reduced renal and vascular dysfunction in response to angiotensin II (Ang II) infusion. Monoclonal antibodies to IL-17 isoforms or the IL-17 receptor are emerging as novel therapeutics for psoriasis and related autoimmune disorders. METHODS AND

resultsMice were infused with Ang II for 4 weeks to induce hypertension. Using flow cytometry and intracellular staining, we determined that the primary T cell subsets producing IL-17A and IL-17F in the kidney and aorta are gamma delta (γδ) T cells and CD4+ T helper 17 (T

conclusionsMonoclonal antibodies to IL-17A or IL-17RA, but not IL-17F, may be a useful adjunct treatment for hypertension and the associated end-organ dysfunction.

Indexed as

angiotensin IIgamma delta T cellshypertensioninterleukin 17Ainterleukin 17Finterleukin 17RA receptorT lymphocytes

Identifiers

PMID28280792
PMCPMC5337944
OpenAlexW2549136953

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.