Evidence map›Paper›PMID 30746505›Full record

ArticleJournal of the Endocrine Society2019

A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling.

Qunsheng Dai, Creighton E Likes, Anthony L Luz, Lan Mao, Jason S Yeh, Zhengzheng Wei, Maragatha Kuchibhatla, Olga R Ilkayeva, Timothy R Koves, Thomas M Price

Open access · goldAbstract read
In one paragraph

Article in Journal of the Endocrine Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  7. Menstruation-Related Angina-The Wee Hours.The International journal of angiology : official publication of the International College of Angiology, Inc · 2024
    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

10 authors at 1 institution in 1 country.

Qunsheng DaiDivision of Reproductive Endocrinology, Duke University, Durham, North Carolina.
Creighton E LikesDivision of Reproductive Endocrinology, Duke University, Durham, North Carolina.
Anthony L LuzNicholas School of the Environment, Duke University, Durham, North Carolina.
Lan MaoDivision of Cardiology, Duke University, Durham, North Carolina.
Jason S YehDivision of Reproductive Endocrinology, Duke University, Durham, North Carolina.
Zhengzheng WeiCenter for Genomic and Computational Biology, Duke University, Durham, North Carolina.
Maragatha KuchibhatlaDivision of Biostatistics and Bioinformatics, Sarah W. Stedman Nutrition and Metabolism Center, Duke University, Durham, North Carolina.
Olga R IlkayevaDuke Molecular Physiology Institute, Duke University, Durham, North Carolina.
Timothy R KovesDuke Molecular Physiology Institute, Duke University, Durham, North Carolina.
Thomas M PriceDivision of Reproductive Endocrinology, Duke University, Durham, North Carolina.ORCID 0000-0002-9720-7416
Duke University · US

Funding

Duke University Program in Environmental HealthT32ES021432 · NIEHS · DUKE UNIVERSITY · PI Akhenaton-Andrew Dhafir Jones, Joel Newman Meyer · 2013 to 2026
$4.0M
Cardiac Effects of a Mitochondrial Progesterone ReceptorR03HD058017 · NICHD · DUKE UNIVERSITY · PI PRICE, THOMAS M · 2008 to 2009
$156k
NICHD NIH HHS R03 HD058017NIEHS NIH HHS T32 ES021432
6 · The paper itself

Abstract

Progesterone is primarily a pregnancy-related hormone, produced in substantial quantities after ovulation and during gestation. Traditionally known to function via nuclear receptors for transcriptional regulation, there is also evidence of nonnuclear action. A previously identified mitochondrial progesterone receptor (PR-M) increases cellular respiration in cell models. In these studies, we demonstrated that expression of PR-M in rat H9c2 cardiomyocytes resulted in a ligand-dependent increase in oxidative cellular respiration and beta-oxidation. Cardiac expression in a TET-On transgenic mouse resulted in gene expression of myofibril proteins for remodeling and proteins involved in oxidative phosphorylation and fatty acid metabolism. In a model of increased afterload from constant transverse aortic constriction, mice expressing PR-M showed a ligand-dependent preservation of cardiac function. From these observations, we propose that PR-M is responsible for progesterone-induced increases in cellular energy production and cardiac remodeling to meet the physiological demands of pregnancy.

Indexed as

beta-oxidationmitochondriapregnancyprogesteronerespiratory chain

Identifiers

PMID30746505
PMCPMC6364628
OpenAlexW2907984525

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.