Evidence map›Paper›PMID 27496559›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2016

Angiotensin type 2 receptor null mice express reduced levels of renal angiotensin II type 2 receptor/angiotensin (1-7)/Mas receptor and exhibit greater high-fat diet-induced kidney injury.

Quaisar Ali, Isha Dhande, Preethi Samuel, Tahir Hussain

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Dimerization of ATCurrent hypertension reports · 2018
    Review
  14. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Quaisar AliDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, USA.
Isha DhandeDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, USA.
Preethi SamuelDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, USA.
Tahir HussainDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, USA thussain@central.uh.edu.
University of Houston · US

Funding

Renal Angiotensin ll Receptor Function in ObesityR01DK061578 · NIDDK · UNIVERSITY OF HOUSTON · PI HUSSAIN, TAHIR · 2003 to 2020
$4.3M
NIDDK NIH HHS R01 DK061578
6 · The paper itself

Abstract

introductionRenin-angiotensin system (RAS) components exert diverse physiological functions and have been sub-grouped into deleterious angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/angiotensin type 1 receptor (AT1R) and protective ACE2/angiotensin (1-7) (Ang-(1-7))/Mas receptor (MasR) axes. We have reported that chronic activation of angiotensin type 2 receptor (AT2R) alters RAS components and provides protection against obesity-related kidney injury. MATERIALS AND

methodsWe utilized AT2R knockout (AT2KO) mice in this study and evaluated the renal expression of various RAS components and examined the renal injury after placing these mice on high fat diet (HFD) for 16 weeks.

resultsThe cortical ACE2 activity and MasR expression were significantly decreased in AT2KO mice compared to wild type (WT) mice. LC/MS analysis revealed an increase in renal Ang II levels and a decrease in Ang-(1-7) levels in AT2KO mice. Cortical expression of ACE and AT1R was increased but renin activity remained unchanged in AT2KO compared with WT mice. WT mice fed HFD exhibited increased systolic blood pressure, higher indices of kidney injury, mesangial matrix expansion score, and microalbuminuria, which were further increased in AT2KO mice.

conclusionThis study suggests that deletion of AT2R decreases the expression of the beneficial ACE2/Ang-(1-7)/MasR and increases the deleterious ACE/Ang II/AT1R axis of the renal RAS in mice. Further, AT2KO mice are more susceptible to HFD-induced renal injury.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAnimalsBiomarkersBlood PressureChromatography, LiquidDiet, High-FatGene DeletionKidneyMaleMass SpectrometryMice, KnockoutPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsAce2 protein, mouseAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)BiomarkersPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 2Receptors, G-Protein-CoupledReninangiotensin (1-7)angiotensin II type 2 receptor knockoutMas receptorRenin–angiotensin system

Identifiers

PMID27496559
PMCPMC5843939
OpenAlexW2494072235

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.