Evidence map›Paper›PMID 24804145›Full record

ReviewInternational journal of inflammation2014

The Renin-Angiotensin-aldosterone system in vascular inflammation and remodeling.

Maricica Pacurari, Ramzi Kafoury, Paul B Tchounwou, Kenneth Ndebele

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

Review in International journal of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 5 pooled it
19.3field-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

206 citing papers in PubMed, 5 syntheses or guidelines pooled it, 370 citations in OpenAlex.

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  10. The gut-heart axis in cardio-oncology.Cardiovascular research · 2026
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146 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.

Maricica PacurariBiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA ; NIH RCMI-Center for Environmental Health, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA.
Ramzi KafouryBiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA ; NIH RCMI-Center for Environmental Health, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA.
Paul B TchounwouBiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA ; NIH RCMI-Center for Environmental Health, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA.
Kenneth NdebeleBiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA ; NIH RCMI-Center for Environmental Health, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USA.
Jackson State University · US

Funding

RCMI-Center for Environmental HealthG12MD007581 · NIMHD · JACKSON STATE UNIVERSITY · PI TCHOUNWOU, PAUL B. · 2012 to 2017
$11.2M
NIMHD NIH HHS G12 MD007581
6 · The paper itself

Abstract

The RAAS through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of CVD such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and its role in hypertension, RAAS has proinflammatory and profibrotic effects at cellular and molecular levels. Blocking RAAS provides beneficial effects for the treatment of cardiovascular and renal diseases. Evidence shows that inhibition of RAAS positively influences vascular remodeling thus improving CVD outcomes. The beneficial vascular effects of RAAS inhibition are likely due to decreasing vascular inflammation, oxidative stress, endothelial dysfunction, and positive effects on regeneration of endothelial progenitor cells. Inflammatory factors such as ICAM-1, VCAM-1, TNFα, IL-6, and CRP have key roles in mediating vascular inflammation and blocking RAAS negatively modulates the levels of these inflammatory molecules. Some of these inflammatory markers are clinically associated with CVD events. More studies are required to establish long-term effects of RAAS inhibition on vascular inflammation, vascular cells regeneration, and CVD clinical outcomes. This review presents important information on RAAS's role on vascular inflammation, vascular cells responses to RAAS, and inhibition of RAAS signaling in the context of vascular inflammation, vascular remodeling, and vascular inflammation-associated CVD. Nevertheless, the review also equates the need to rethink and rediscover new RAAS inhibitors.

Identifiers

PMID24804145
PMCPMC3997861
OpenAlexW2051926037

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.