Evidence map›Paper›PMID 28571891›Full record

ReviewPharmacological research2017

Renin angiotensin aldosterone inhibition in the treatment of cardiovascular disease.

Carlos M Ferrario, Adam E Mullick

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
9.3field-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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

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  20. DNA Methylation of the Angiotensinogen Gene,International journal of molecular sciences · 2021
    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 2 institutions in 1 country.

Carlos M FerrarioDepartment of Surgery, Wake Forest University Health Science, Medical Center Blvd., Winston Salem, NC 27157, United States. Electronic address: cferrari@wakehealth.edu.
Adam E MullickCardiovascular Antisense Drug Discovery, Ionis Pharmaceuticals, Inc., Carlsbad, CA 92010, United States.
Ionis Pharmaceuticals (United States) · USWake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FERRARIO, CARLOS M · 1994 to 2019
$34.8M
NHLBI NIH HHS P01 HL051952
6 · The paper itself

Abstract

A collective century of discoveries establishes the importance of the renin angiotensin aldosterone system in maintaining blood pressure, fluid volume and electrolyte homeostasis via autocrine, paracrine and endocrine signaling. While research continues to yield new functions of angiotensin II and angiotensin-(1-7), the gap between basic research and clinical application of these new findings is widening. As data accumulates on the efficacy of angiotensin converting enzyme inhibitors and angiotensin II receptor blockers as drugs of fundamental importance in the treatment of cardiovascular and renal disorders, it is becoming apparent that the achieved clinical benefits is suboptimal and surprisingly no different than what can be achieved with other therapeutic interventions. We discuss this issue and summarize new pathways and mechanisms effecting the synthesis and actions of angiotensin II. The presence of renin-independent non-canonical pathways for angiotensin II production are largely unaffected by agents inhibiting renin angiotensin system activity. Hence, new efforts should be directed to develop drugs that can effectively block the synthesis and/or action of intracellular angiotensin II. Improved drug penetration into cardiac or renal sites of disease, inhibiting chymase the primary angiotensin II forming enzyme in the human heart, and/or inhibiting angiotensinogen synthesis would all be more effective strategies to inhibit the system. Additionally, given the role of angiotensin II in the maintenance of renal homeostatic mechanisms, any new inhibitor should possess greater selectivity of targeting pathogenic angiotensin II signaling processes and thereby limit inappropriate inhibition.

Indexed as

AldosteroneAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsAnimalsCardiovascular DiseasesHumansReninRenin-Angiotensin SystemAldosteroneAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsReninAngiotensin-(1–12)Angiotensin-(1–7)Angiotensin converting enzyme inhibitorsAngiotensin receptor blockersHeart failureHypertension

Identifiers

PMID28571891
PMCPMC5648016
OpenAlexW2618061614

What Socratic 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 Socratic graph.