Evidence map›Paper›PMID 33789143›Full record

ReviewMolecular and cellular endocrinology2021

Advances in use of mouse models to study the renin-angiotensin system.

Jacqueline M Emathinger, Jonathan W Nelson, Susan B Gurley

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
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

3 authors.

Jacqueline M EmathingerDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR, USA. Electronic address: emathing@ohsu.edu.
Jonathan W NelsonDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR, USA. Electronic address: nelsonjo@ohsu.edu.
Susan B GurleyDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR, USA. Electronic address: gurley@ohsu.edu.

Funding

Oregon Clinical and Translational Research Institute TL1 ProgramTL1TR002371 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ALLISON Deborah FRYER, JESSINA C MCGREGOR · 2017 to 2026
$6.2M
Actions of Angiotensin II Along the Nephron to Regulate Blood PressureR01DK098382 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GURLEY, SUSAN BAILEY · 2014 to 2025
$3.8M
Medical Scientist Training Program of Oregon Health & Science UniversityT32GM109835 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI JACOBY, DAVID B · 2016 to 2020
$1.1M
Renal Pericytes as a Target for Angiotensin II Signaling in HypertensionK01DK121737 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI NELSON, JONATHAN W · 2020 to 2024
$669k
NCATS NIH HHS TL1 TR002371NIDDK NIH HHS K01 DK121737NIDDK NIH HHS R01 DK098382NIGMS NIH HHS T32 GM109835
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) is a highly complex hormonal cascade that spans multiple organs and cell types to regulate solute and fluid balance along with cardiovascular function. Much of our current understanding of the functions of the RAS has emerged from a series of key studies in genetically-modified animals. Here, we review key findings from ground-breaking transgenic models, spanning decades of research into the RAS, with a focus on their use in studying blood pressure. We review the physiological importance of this regulatory system as evident through the examination of mouse models for several major RAS components: angiotensinogen, renin, ACE, ACE2, and the type 1 A angiotensin receptor. Both whole-animal and cell-specific knockout models have permitted critical RAS functions to be defined and demonstrate how redundancy and multiplicity within the RAS allow for compensatory adjustments to maintain homeostasis. Moreover, these models present exciting opportunities for continued discovery surrounding the role of the RAS in disease pathogenesis and treatment for cardiovascular disease and beyond.

Indexed as

Disease Models, AnimalAngiotensin-Converting Enzyme 2AngiotensinogenAnimalsBlood PressureCardiovascular DiseasesGene Expression RegulationHumansKidneyMiceMice, KnockoutReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2ReninRenin-Angiotensin SystemSignal TransductionAce2 protein, mouseAngiotensin-Converting Enzyme 2AngiotensinogenReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2ReninACEACE2AT1RCell-specific knockout miceMouse models

Identifiers

PMID33789143
PMCPMC9119406

What Socratic holds

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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.