Evidence map›Paper›PMID 21266264›Full record

ArticleSeminars in nephrology2011

Renin angiotensin signaling in normal pregnancy and preeclampsia.

Roxanna A Irani, Yang Xia

Open access · greenAbstract read
In one paragraph

Article in Seminars in nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Cardiovascular complications of pregnancy.The Journal of clinical investigation · 2026
    Review
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  6. Article
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  12. Article
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  17. Glomerular hyperfiltration.Nature reviews. Nephrology · 2022
    Review
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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

2 authors at 1 institution in 1 country.

Roxanna A IraniDepartment of Biochemistry & Molecular Biology, University of Texas at Houston Medical School, 6431 Fannin Street, Houston, TX 77030, USA.
Yang Xia
The University of Texas Health Science Center at Houston · US

Funding

AT1 Receptor Activating Autoantibodies and PreeclampsiaR01HL076558 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI XIA, YANG · 2005 to 2008
$1.0M
NHLBI NIH HHS R01 HL076558
6 · The paper itself

Abstract

Many reports indicate that there is an increase in almost all of the components of the renin-angiotensin system (RAS) during an uncomplicated pregnancy, but renin activity, angiotensin II, and aldosterone decrease in preeclampsia (PE) for reasons that are unclear. PE is a life-threatening disorder of late pregnancy characterized by hypertension, proteinuria, increased soluble fms-like tyrosine kinase-1, as well as renal and placental morphologic abnormalities. Although a leading cause of maternal and perinatal morbidity and mortality, the pathogenic mechanisms of PE remain largely undefined. Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder. Bridging these two concepts, numerous studies report the presence of the angiotensin II type I receptor agonistic autoantibody (AT(1)-AA) found circulating in preeclamptic women. This autoantibody induces many key features of the disorder through AT(1) receptor signaling, and has been implicated in the pathogenesis of PE. Here we review the functions of the RAS during normal pregnancy and PE, and highlight the role of AT(1)-AA in both animal models and in the human disorder.

Indexed as

Angiotensin IIAnimalsAutoantibodiesFemaleHumansModels, AnimalPre-EclampsiaPregnancyReceptor, Angiotensin, Type 1Renin-Angiotensin SystemSignal TransductionAngiotensin IIAutoantibodiesReceptor, Angiotensin, Type 1

Identifiers

PMID21266264
PMCPMC3275085
OpenAlexW2106742477

What OpenQuestion holds

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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.