Evidence map›Paper›PMID 24163075›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2014

Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension.

Cameron G McCarthy, Styliani Goulopoulou, Camilla F Wenceslau, Kathryn Spitler, Takayuki Matsumoto, R Clinton Webb

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Sex differences in TLR4 expression in SHR do not contribute to sex differences in blood pressure or the renal T cell profile.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Trial
  3. Trial
  4. Review
  5. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Markers of Vascular Dysfunction in Hypertension.Current medicinal chemistry · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Biology · 2023
    Article
  20. Review

38 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 3 institutions in 2 countries.

Cameron G McCarthyDepartment of Physiology, Georgia Regents University, Augusta, Georgia; and.
Styliani Goulopoulou
Camilla F Wenceslau
Kathryn Spitler
Takayuki Matsumoto
R Clinton Webb
Augusta University · USGeorgia Regents Medical Center · USHoshi University · JP

Funding

Nitric Oxide Inhibits RhoA/Rho-kinase in Penile ErectionR01HL071138 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WEBB, R CLINTON · 2003 to 2011
$2.9M
TNF-alpha: a key player in erectile (dys)functionR01DK083685 · NIDDK · AUGUSTA UNIVERSITY · PI WEBB, R CLINTON · 2009 to 2012
$1.4M
NHLBI NIH HHS R01 HL-071138NIDDK NIH HHS R01 DK-083685
6 · The paper itself

Abstract

Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible changes to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.

Indexed as

AnimalsEndothelium, VascularHumansHypertensionImmunity, InnateInflammationMuscle, Smooth, VascularToll-Like ReceptorsToll-Like Receptorsinnate immunityvascular dysfunctionvascular remodeling

Identifiers

PMID24163075
PMCPMC3920129
OpenAlexW2169848995

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.