Evidence map›Paper›PMID 23785077›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2013

Cortisol stimulates proliferation and apoptosis in the late gestation fetal heart: differential effects of mineralocorticoid and glucocorticoid receptors.

Xiaodi Feng, Seth A Reini, Elaine Richards, Charles E Wood, Maureen Keller-Wood

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Chronic maternal hypercortisolemia models stress-induced adverse birth outcome and altered cardiac function in newborn lambs.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  8. Article
  9. Sodium dichloroacetate stimulates cardiac mitochondrial metabolism and improves cardiac conduction in the ovine fetus during labor.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  10. Review
  11. Maternal hypercortisolemia alters placental metabolism: a multiomics view.American journal of physiology. Endocrinology and metabolism · 2020
    Article
  12. Article
  13. Transcriptomic evidence that cortisol alters perinatal epicardial adipose tissue maturation.American journal of physiology. Endocrinology and metabolism · 2019
    Article
  14. Article
  15. Mechanisms of in utero cortisol effects on the newborn heart revealed by transcriptomic modeling.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Xiaodi FengDepartments of Pharmacodynamics, and Physiology and Functional Genomics, University of Florida, Gainesville, Florida.
Seth A Reini
Elaine Richards
Charles E Wood
Maureen Keller-Wood
University of Florida · US

Funding

Effects of maternal cortisol on fetal and neonatal growth and metabolismR01HD057871 · NICHD · UNIVERSITY OF FLORIDA · PI KELLER-WOOD, MAUREEN · 2009 to 2013
$1.5M
Cortisol at MR Mediate Fetal Physiologic/Genomic EffectsR01DK062080 · NIDDK · UNIVERSITY OF FLORIDA · PI KELLER-WOOD, MAUREEN · 2003 to 2007
$1.5M
NICHD NIH HHS HD-057871NICHD NIH HHS R01 HD057871NIDDK NIH HHS DK-62080NIDDK NIH HHS R01 DK062080
6 · The paper itself

Abstract

We have previously found that modest chronic increases in maternal cortisol result in an enlarged fetal heart. To explore the mechanisms of this effect, we used intrapericardial infusions of a mineralocorticoid receptor (MR) antagonist (canrenoate) or of a glucocorticoid receptor (GR) antagonist (mifepristone) in the fetus during maternal infusion of cortisol (1 mg·kg⁻¹·day⁻¹). We have shown that the MR antagonist blocked the increase in fetal heart weight and in wall thickness resulting from maternal cortisol infusion. In the current study we extended those studies and found that cortisol increased Ki67 staining in both ventricles, indicating cell proliferation, but also increased active caspase-3 staining in cells of the conduction pathway in the septum and subendocardial layers of the left ventricle, suggesting increased apoptosis in Purkinje fibers. The MR antagonist blocked the increase in cell proliferation, whereas the GR antagonist blocked the increased apoptosis in Purkinje fibers. We also found evidence of activation of caspase-3 in c-kit-positive cells, suggesting apoptosis in stem cell populations in the ventricle. These studies suggest a potentially important role of corticosteroids in the terminal remodeling of the late gestation fetal heart and suggest a mechanism for the cardiac enlargement with excess corticosteroid exposure.

Indexed as

AnimalsApoptosisCanrenoic AcidCardiomegalyCaspase 3Cell ProliferationFemaleFetal HeartGestational AgeHydrocortisoneInfusions, IntravenousKi-67 AntigenMifepristoneMineralocorticoid Receptor AntagonistsPregnancyProto-Oncogene Proteins c-kitCanrenoic AcidCaspase 3HydrocortisoneKi-67 AntigenMifepristoneMineralocorticoid Receptor AntagonistsProto-Oncogene Proteins c-kitReceptors, GlucocorticoidReceptors, Mineralocorticoidcardiomyocytecaspase-3Purkinje fibersheepstress

Identifiers

PMID23785077
PMCPMC3833392
OpenAlexW2165533896

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.