Evidence map›Paper›PMID 29186034›Full record

ReviewInternational journal of molecular sciences2017

Cellular and Oxidative Mechanisms Associated with Interleukin-6 Signaling in the Vasculature.

Sean P Didion

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

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 4 pooled it
5.4field-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

147 citing papers in PubMed, 4 syntheses or guidelines pooled it, 216 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Observational
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Observational
  15. Review
  16. The burden of cardiovascular disease in prostate cancer: prevalence, pathophysiology, and implications for integrated care.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Review
  17. Article
  18. Article
  19. Article
  20. Review

87 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

1 author at 1 institution in 1 country.

Sean P DidionDepartments of Pharmacology and Neurology, The University of Mississippi Medical Center, Arthur C. Guyton Laboratory Research Building, Jackson, MS 39216, USA. didionlab@gmail.com.
University of Mississippi Medical Center · US

Funding

Molecular Mechanisms of Hypertension in the MicrocirculationR01HL107632 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI DIDION, SEAN P · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL107632
6 · The paper itself

Abstract

Reactive oxygen species, particularly superoxide, promote endothelial dysfunction and alterations in vascular structure. It is increasingly recognized that inflammatory cytokines, such as interleukin-6 (IL-6), contribute to endothelial dysfunction and vascular hypertrophy and fibrosis. IL-6 is increased in a number of cardiovascular diseases, including hypertension. IL-6 is also associated with a higher incidence of future cardiovascular events and all-cause mortality. Both immune and vascular cells produce IL-6 in response to a number of stimuli, such as angiotensin II. The vasculature is responsive to IL-6 produced from vascular and non-vascular sources via classical IL-6 signaling involving a membrane-bound IL-6 receptor (IL-6R) and membrane-bound gp130 via Jak/STAT as well as SHP2-dependent signaling pathways. IL-6 signaling is unique because it can also occur via a soluble IL-6 receptor (sIL-6R) which allows for IL-6 signaling in tissues that do not normally express IL-6R through a process referred to as IL-6 trans-signaling. IL-6 signaling mediates a vast array of effects in the vascular wall, including endothelial activation, vascular permeability, immune cell recruitment, endothelial dysfunction, as well as vascular hypertrophy and fibrosis. Many of the effects of IL-6 on vascular function and structure are representative of loss or reductions in nitric oxide (NO) bioavailability. IL-6 has direct effects on endothelial nitric oxide synthase activity and expression as well as increasing vascular superoxide, which rapidly inactivates NO thereby limiting NO bioavailability. The goal of this review is to highlight both the cellular and oxidative mechanisms associated with IL-6-signaling in the vascular wall in general, in hypertension, and in response to angiotensin II.

Indexed as

AnimalsHumansInterleukin-6NADPH OxidasesNitric Oxide Synthase Type IIISignal TransductionSuperoxidesInterleukin-6NADPH OxidasesNitric Oxide Synthase Type IIISuperoxidesangiotensin IIendothelial nitric oxide synthaseinflammationNADPH oxidasesuperoxidevascular biology

Identifiers

PMID29186034
PMCPMC5751166
OpenAlexW2775702351

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.