Evidence map›Paper›PMID 29321064›Full record

ArticleReproductive biology and endocrinology : RB&E2017

The role of ACE2, angiotensin-(1-7) and Mas1 receptor axis in glucocorticoid-induced intrauterine growth restriction.

Elham Ghadhanfar, Aseel Alsalem, Shaimaa Al-Kandari, Jumana Naser, Fawzi Babiker, Maie Al-Bader

RetractedOpen access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

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  15. ACE2: a key modulator of the renin-angiotensin system and pregnancy.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Elham GhadhanfarDepartment of Physiology, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Aseel AlsalemFaculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Shaimaa Al-KandariFaculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Jumana NaserFaculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Fawzi BabikerDepartment of Physiology, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait.
Maie Al-BaderDepartment of Physiology, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait. albader@hsc.edu.kw.
Kuwait University · KW

Funding

Kuwait University MY02/15
6 · The paper itself

Abstract

backgroundPlasma and urine levels of the potent vasodilator Ang-(1-7) are elevated in mid and late pregnancy and are correlated with elevated placental angiogenesis, fetal blood flow, and rapid fetal growth. We hypothesized that Ang-(1-7), its receptor (Mas1) and the enzymes involved in Ang-(1-7) production (ACE2 and Membrane metallo-endopeptidase; MME) are down regulated in response to glucocorticoid administration contributing to IUGR.

methodsPregnant female Sprague-Dawley rats were injected with dexamethasone (DEX; 0.4 mg/kg/day) starting from 14 day gestation (dg) till sacrifice at 19 or 21 dg while control groups were injected with saline (n = 6/group). The gene and protein expression of ACE2, MME, Ang-(1-7) and Mas1 receptor in the placental labyrinth (LZ) and basal zones (BZ) were studied.

resultsDEX administration caused a reduction in LZ weight at 19 and 21 dg (p < 0.001). IUGR, as shown by decreased fetal weights, was evident in DEX treated rats at 21 dg (p < 0.01). ACE2 gene expression was elevated in the LZ of control placentas at 21 dg (p < 0.01) compared to 19 dg and DEX prevented this rise at both gene (p < 0.01) and protein levels (p < 0.05). In addition, Ang-(1-7) protein expression in LZ was significantly reduced in DEX treated rats at 21 dg (p < 0.05). On the other hand, Mas1 and MME were upregulated in LZ at 21 dg in both groups (p < 0.05 and p < 0.001, respectively).

conclusionThe results of this study indicate that a reduced expression of ACE2 and Ang-(1-7) in the placenta by DEX treatment may be responsible for IUGR and consequent disease programming later in life.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAnimalsDexamethasoneFemaleFetal Growth RetardationGlucocorticoidsPeptide FragmentsPeptidyl-Dipeptidase APlacentaPregnancyProto-Oncogene MasProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)DexamethasoneGlucocorticoidsMas1 protein, ratPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledACE2Ang-(1–7)DexamethasoneIUGRMas1 receptorMME

Identifiers

PMID29321064
PMCPMC6389120
OpenAlexW2783504280

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.