Evidence map›Paper›PMID 32114685›Full record

ReviewCurrent hypertension reports2020

Recent Research Advances in Renin-Angiotensin-Aldosterone System Receptors.

Kengo Azushima, Norihiko Morisawa, Kouichi Tamura, Akira Nishiyama

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Direct Vascular Effects of Angiotensin II (A Systematic Short Review).International journal of molecular sciences · 2024
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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.

Kengo AzushimaCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-5136-0730
Norihiko MorisawaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Takamatsu, Kagawa, Japan.ORCID 0000-0002-1761-3888
Kouichi TamuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.ORCID 0000-0002-0660-5372
Akira NishiyamaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Takamatsu, Kagawa, Japan. akira@med.kagawa-u.ac.jp.ORCID 0000-0001-5971-820X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe renin-angiotensin-aldosterone system (RAAS) plays important roles in regulating blood pressure and body fluid, which contributes to the pathophysiology of hypertension and cardiovascular/renal diseases. However, accumulating evidence has further revealed the complexity of this signal transduction system, including direct interactions with other receptors and proteins. This review focuses on recent research advances in RAAS with an emphasis on its receptors. RECENT

findingsBoth systemically and locally produced angiotensin II (Ang II) bind to Ang II type 1 receptor (AT1R) and elicit strong biological functions. Recent studies have shown that Ang II-induced activation of Ang II type 2 receptor (AT2R) elicits the opposite functions to those of AT1R. However, accumulating evidence has now expanded the components of RAAS, including (pro)renin receptor, angiotensin-converting enzyme 2, angiotensin 1-7, and Mas receptor. In addition, the signal transductions of AT1R and AT2R are regulated by not only Ang II but also its receptor-associated proteins such as AT1R-associated protein and AT2R-interacting protein. Recent studies have indicated that inappropriate activation of local mineralocorticoid receptor contributes to cardiovascular and renal tissue injuries through aldosterone-dependent and -independent mechanisms. Since the mechanisms of RAAS signal transduction still remain to be elucidated, further investigations are necessary to explore novel molecular mechanisms of the RAAS, which will provide alternative therapeutic agents other than existing RAAS blockers.

Indexed as

HypertensionReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Renin-Angiotensin SystemAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensin II Type 2 Receptor BlockersHumansProto-Oncogene MasAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensin II Type 2 Receptor BlockersMAS1 protein, humanProto-Oncogene MasReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Angiotensin type 1 receptor (AT1R)Angiotensin type 2 receptor (AT2R)Mas receptor (MasR)Mineralocorticoid receptor (MR)(Pro)renin receptor (PRR)

Identifiers

What Socratic 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 Socratic graph.