Evidence map›Paper›PMID 34206708›Full record

ReviewInternational journal of molecular sciences2021

Renin-Angiotensin System in Pathogenesis of Atherosclerosis and Treatment of CVD.

Anastasia V Poznyak, Dwaipayan Bharadwaj, Gauri Prasad, Andrey V Grechko, Margarita A Sazonova, Alexander N Orekhov

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 4 pooled it
13.7field-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

75 citing papers in PubMed, 4 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
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  3. Direct Vascular Effects of Angiotensin II (A Systematic Short Review).International journal of molecular sciences · 2024
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15 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 4 institutions in 2 countries.

Anastasia V PoznyakInstitute for Atherosclerosis Research, Skolkovo Innovative Center, 121609 Moscow, Russia.ORCID 0000-0002-1516-1320
Dwaipayan BharadwajAcademy of Scientific and Innovative Research, CSIR-Institute of Genomics and Integrative Biology Campus, New Delhi 110067, India.
Gauri PrasadSystems Genomics Laboratory, School of Biotechnology, Jawaharlal Nehru University, New Delhi 110067, India.
Andrey V GrechkoFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 14-3 Solyanka Street, 109240 Moscow, Russia.
Margarita A SazonovaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.ORCID 0000-0002-8610-4593
Alexander N OrekhovInstitute for Atherosclerosis Research, Skolkovo Innovative Center, 121609 Moscow, Russia.ORCID 0000-0002-3318-4681
Jawaharlal Nehru University · INResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUInstitute for Atherosclerosis Research · RUV.A. Negovsky Scientific Research Institute of General Reanimatology · RU

Funding

Russian Science Foundation 20-15-00364
6 · The paper itself

Abstract

Atherosclerosis has complex pathogenesis, which involves at least three serious aspects: inflammation, lipid metabolism alterations, and endothelial injury. There are no effective treatment options, as well as preventive measures for atherosclerosis. However, this disease has various severe complications, the most severe of which is cardiovascular disease (CVD). It is important to note, that CVD is among the leading causes of death worldwide. The renin-angiotensin-aldosterone system (RAAS) is an important part of inflammatory response regulation. This system contributes to the recruitment of inflammatory cells to the injured site and stimulates the production of various cytokines, such as IL-6, TNF-a, and COX-2. There is also an association between RAAS and oxidative stress, which is also an important player in atherogenesis. Angiotensin-II induces plaque formation at early stages, and this is one of the most crucial impacts on atherogenesis from the RAAS. Importantly, while stimulating the production of ROS, Angiotensin-II at the same time decreases the generation of NO. The endothelium is known as a major contributor to vascular function. Oxidative stress is the main trigger of endothelial dysfunction, and, once again, links RAAS to the pathogenesis of atherosclerosis. All these implications of RAAS in atherogenesis lead to an explicable conclusion that elements of RAAS can be promising targets for atherosclerosis treatment. In this review, we also summarize the data on treatment approaches involving cytokine targeting in CVD, which can contribute to a better understanding of atherogenesis and even its prevention.

Indexed as

Disease SusceptibilityRenin-Angiotensin SystemAngiotensin-Converting Enzyme InhibitorsAnimalsAtherosclerosisBiomarkersCardiovascular DiseasesClinical Trials as TopicDisease ManagementDrug Evaluation, PreclinicalEndotheliumHumansMolecular Targeted TherapyOxidative StressReactive Oxygen SpeciesAngiotensin-Converting Enzyme InhibitorsBiomarkersReactive Oxygen SpeciesatherosclerosisCVDRAASrenin–angiotensin–aldosterone system

Identifiers

PMID34206708
PMCPMC8269397
OpenAlexW3177117624

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.