Evidence map›Paper›PMID 31325339›Full record

ReviewExperimental physiology2019

Inflammation as a mediator of arterial ageing.

Daniel W Trott, Paul J Fadel

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024
    Review
  4. Article
  5. Immunomodulation in age-related disorders and nanotechnology interventions.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Endothelium as a Source and Target of HAntioxidants (Basel, Switzerland) · 2021
    Review
  10. Review
  11. 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

2 authors at 1 institution in 1 country.

Daniel W TrottDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.ORCID 0000-0003-4872-4422
Paul J FadelDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.ORCID 0000-0002-5084-2666
The University of Texas at Arlington · US

Funding

Targeting Sympathetic Overactivity in CKD patients: Mechanisms & Novel TherapiesR01HL127071 · NHLBI · UNIVERSITY OF TEXAS ARLINGTON · PI FADEL, PAUL J · 2016 to 2019
$1.7M
T cells mediate age related arterial dysfunctionK01AG061271 · NIA · UNIVERSITY OF TEXAS ARLINGTON · PI TROTT, DANIEL · 2019 to 2023
$635k
Sympathetic baroreflex control and vascular transduction in African AmericansR15HL130906 · NHLBI · UNIVERSITY OF TEXAS ARLINGTON · PI KELLER, DAVID M · 2016 to 2016
$377k
NHLBI NIH HHS R01 HL127071NHLBI NIH HHS R15 HL130906NIA NIH HHS K01 AG061271
6 · The paper itself

Abstract

NEW

findingsWhat is the topic of this review? This review summarizes and synthesizes what is known about the contribution of inflammation to age-related arterial dysfunction. What advances does it highlight? This review details observational evidence for the relationship of age-related inflammation and arterial dysfunction, insight from autoimmune inflammatory diseases and their effects on arterial function, interventional evidence linking inflammation and age-related arterial dysfunction, insight into age-related arterial inflammation from preclinical models and interventions to ameliorate age-related inflammation and arterial dysfunction. ABSTRACT: Advanced age is a primary risk factor for cardiovascular disease, the leading cause of death in the industrialized world. Two major components of arterial ageing are stiffening of the large arteries and impaired endothelium-dependent dilatation in multiple vascular beds. These two alterations are major contributors to the development of overt cardiovascular disease. Increasing inflammation with advanced age is likely to play a role in this arterial dysfunction. The purpose of this review is to synthesize what is known about inflammation and its relationship to age-related arterial dysfunction. This review discusses both the initial observational evidence for the relationship of age-related inflammation and arterial dysfunction and the evidence that inflammatory autoimmune diseases are associated with a premature arterial ageing phenotype. We next discuss interventional and mechanistic evidence linking inflammation and age-related arterial dysfunction in older adults. We also attempt to summarize the relevant evidence from preclinical models. Lastly, we discuss interventions in both humans and animals that have been shown to ameliorate age-related arterial inflammation and dysfunction. The available evidence provides a strong basis for the role of inflammation in both large artery stiffening and impairment of endothelium-dependent dilatation; however, the specific inflammatory mediators, the initiating factors and the relative importance of the endothelium, smooth muscle cells, perivascular adipose tissue and immune cells in arterial inflammation are not well understood. With the expansion of the ageing population, ameliorating age-related arterial inflammation represents an important potential strategy for preserving vascular health in the elderly.

Indexed as

AgingAnimalsArteriesCardiovascular DiseasesEndothelium, VascularHumansInflammationageingendotheliumperivascular adipose tissuesmooth musclevascular

Identifiers

PMID31325339
PMCPMC6773510
OpenAlexW2964034787

What OpenQuestion holds

Textmetadata
LicenceTDM
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.