Evidence map›Paper›PMID 22170620›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2012

Novel roles of nuclear angiotensin receptors and signaling mechanisms.

TanYa M Gwathmey, Ebaa M Alzayadneh, Karl D Pendergrass, Mark C Chappell

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  17. Mitochondrial angiotensin receptors and cardioprotective pathways.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  18. Article
  19. Article
  20. Review

9 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

4 authors at 1 institution in 1 country.

TanYa M GwathmeyThe Hypertension and Vascular Research Center, Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1032, USA.
Ebaa M Alzayadneh
Karl D Pendergrass
Mark C Chappell
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
The Impact of Antenatal Steroid Exposure on the Intrarenal Renin-Angiotensin SystP01HD047584 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 2005 to 2016
$13.0M
FETAL ENDOCRINE-CARDIOVASCULAR RELATIONSHIPSR01HD017644 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 1985 to 2011
$2.8M
Estrogen, ACE2 and Salt-SensitivityR01HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 2004 to 2008
$1.6M
Establishment of a model for diabetic cardiorenal syndrome in female mRen2.LewisR21HL112237 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, VARAGIC, JASMINA · 2012 to 2013
$398k
REGULATION AND FUNCTION OF ANGIOTENSIN (1-7)R29HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 1996 to 1999
–
NHLBI NIH HHS HL-112237NHLBI NIH HHS HL-51952NHLBI NIH HHS HL-56973NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R01 HL056973NHLBI NIH HHS R21 HL112237NHLBI NIH HHS R29 HL056973NICHD NIH HHS HD-017644NICHD NIH HHS HD-047584NICHD NIH HHS P01 HD047584NICHD NIH HHS R01 HD017644
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) constitutes an important hormonal system in the physiological regulation of blood pressure. The dysregulation of the RAS is considered a major influence in the development and progression of cardiovascular disease and other pathologies. Indeed, experimental and clinical evidence indicates that blockade of this system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin type 1 receptor (AT1R) antagonists is an effective therapy to attenuate hypertension and diabetic renal injury, and to improve heart failure. Originally defined as a circulating system, multiple tissues express a complete RAS, and compelling evidence now favors an intracellular system involved in cell signaling and function. Within the kidney, intracellular expression of the three predominant ANG receptor subtypes is evident in the nuclear compartment. The ANG type 1 receptor (AT1R) is coupled to the generation of reactive oxygen species (ROS) through the activation of phosphoinositol-3 kinase (PI3K) and PKC. In contrast, both ANG type 2 (AT2R) and ANG-(1-7) (AT7R) receptors stimulate nitric oxide (NO) formation, which may involve nuclear endothelial NO synthase (eNOS). Moreover, blockade of either ACE2-the enzyme that converts ANG II to ANG-(1-7)-or the AT7 receptor exacerbates the ANG II-ROS response on renal nuclei. Finally, in a model of fetal programmed hypertension, the nuclear ROS response to ANG II is enhanced, while both AT2 and AT7 stimulation of NO is attenuated, suggesting that an imbalance in the intracellular RAS may contribute to the development of programming events. We conclude that a functional intracellular or nuclear RAS may have important implications in the therapeutic approaches to cardiovascular disease.

Indexed as

AnimalsCell NucleusDisease Models, AnimalHumansHypertensionKidneyMiceRatsReceptors, AngiotensinRenin-Angiotensin SystemSheepSignal TransductionWater-Electrolyte BalanceReceptors, Angiotensin

Identifiers

PMID22170620
PMCPMC3311515
OpenAlexW2051943841

What OpenQuestion 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 OpenQuestion graph.