Evidence map›Paper›PMID 24760441›Full record

ReviewCurrent hypertension reports2014

Angiotensin II and vascular injury.

Augusto C Montezano, Aurelie Nguyen Dinh Cat, Francisco J Rios, Rhian M Touyz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 1 pooled it
16.2field-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

188 citing papers in PubMed, 1 synthesis or guideline pooled it, 394 citations in OpenAlex.

  1. Direct Vascular Effects of Angiotensin II (A Systematic Short Review).International journal of molecular sciences · 2024
    Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. NOR-1 as a Context-Dependent Rheostat of Vascular and Cardiac Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  8. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
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  18. Article
  19. Article
  20. Review

128 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

4 authors at 1 institution in 1 country.

Augusto C MontezanoInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Aurelie Nguyen Dinh Cat
Francisco J Rios
Rhian M Touyz
University of Glasgow · GB

Funding

British Heart FoundationCanadian Institutes of Health Research
6 · The paper itself

Abstract

Vascular injury, characterized by endothelial dysfunction, structural remodelling, inflammation and fibrosis, plays an important role in cardiovascular diseases. Cellular processes underlying this include altered vascular smooth muscle cell (VSMC) growth/apoptosis, fibrosis, increased contractility and vascular calcification. Associated with these events is VSMC differentiation and phenotypic switching from a contractile to a proliferative/secretory phenotype. Inflammation, associated with macrophage infiltration and increased expression of redox-sensitive pro-inflammatory genes, also contributes to vascular remodelling. Among the many factors involved in vascular injury is Ang II. Ang II, previously thought to be the sole biologically active downstream peptide of the renin-angiotensin system (RAS), is converted to smaller peptides, [Ang III, Ang IV, Ang-(1-7)], that are functional and that modulate vascular tone and structure. The actions of Ang II are mediated via signalling pathways activated upon binding to AT1R and AT2R. AT1R activation induces effects through PLC-IP3-DAG, MAP kinases, tyrosine kinases, tyrosine phosphatases and RhoA/Rho kinase. Ang II elicits many of its (patho)physiological actions by stimulating reactive oxygen species (ROS) generation through activation of vascular NAD(P)H oxidase (Nox). ROS in turn influence redox-sensitive signalling molecules. Here we discuss the role of Ang II in vascular injury, focusing on molecular mechanisms and cellular processes. Implications in vascular remodelling, inflammation, calcification and atherosclerosis are highlighted.

Indexed as

Angiotensin IIAnimalsAtherosclerosisCardiovascular DiseasesHumansHypertensionMuscle, Smooth, VascularOxidation-ReductionReactive Oxygen SpeciesRenin-Angiotensin SystemSignal TransductionVascular RemodelingVascular System InjuriesAngiotensin IIReactive Oxygen Species

Identifiers

PMID24760441
OpenAlexW2032831426

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.