Evidence map›Paper›PMID 26986453›Full record

ArticleAutophagy2016

Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model.

Sribalasubashini Muralimanoharan, Xiaoli Gao, Susan Weintraub, Leslie Myatt, Alina Maloyan

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.2field-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

45 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
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  13. The Placenta's Role in Sexually Dimorphic Fetal Growth Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  14. Article
  15. Homeostasis Maintenance inFrontiers in immunology · 2022
    Article
  16. Article
  17. Autophagy and the hallmarks of aging.Ageing research reviews · 2021
    Review
  18. Article
  19. Article
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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

5 authors at 2 institutions in 1 country.

Sribalasubashini Muralimanoharana Center for Pregnancy and Newborn Research , Department of Obstetrics and Gynecology , University of Texas Health Science Center , San Antonio , TX , USA.
Xiaoli Gaob The Metabolomics Core Facility, Institutional Mass Spectrometry Laboratory, University of Texas Health Science Center , San Antonio , TX , USA.
Susan Weintraubb The Metabolomics Core Facility, Institutional Mass Spectrometry Laboratory, University of Texas Health Science Center , San Antonio , TX , USA.
Leslie Myatta Center for Pregnancy and Newborn Research , Department of Obstetrics and Gynecology , University of Texas Health Science Center , San Antonio , TX , USA.
Alina Maloyana Center for Pregnancy and Newborn Research , Department of Obstetrics and Gynecology , University of Texas Health Science Center , San Antonio , TX , USA.
The University of Texas Health Science Center at San Antonio · USOregon Health & Science University · US

Funding

INSTITUTE FOR INTEGRATION OF MEDICINE & SCIENCE: A PARTNERSHIP TO IMPROVE HEALTHUL1RR025767 · NCRR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2008 to 2011
$23.8M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Role of miR-210 in placental mitochondrial metabolismR01HD076259 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MALOYAN, ALINA, MYATT, LESLIE · 2013 to 2017
$1.6M
NCATS NIH HHS UL1 TR001120NCRR NIH HHS UL1 RR025767NICHD NIH HHS R01 HD076259
6 · The paper itself

Abstract

The incidence of maternal obesity and its co-morbidities (diabetes, cardiovascular disease) continues to increase at an alarming rate, with major public health implications. In utero exposure to maternal obesity has been associated with development of cardiovascular and metabolic diseases in the offspring as a result of developmental programming. The placenta regulates maternal-fetal metabolism and shows significant changes in its function with maternal obesity. Autophagy is a cell-survival process, which is responsible for the degradation of damaged organelles and misfolded proteins. Here we show an activation of autophagosomal formation and autophagosome-lysosome fusion in placentas of males but not females from overweight (OW) and obese (OB) women vs. normal weight (NW) women. However, total autophagic activity in these placentas appeared to be decreased as it showed an increase in SQSTM1/p62 and a decrease in lysosomal biogenesis. A mouse model with a targeted deletion of the essential autophagy gene Atg7 in placental tissue showed significant placental abnormalities comparable to those seen in human placenta with maternal obesity. These included a decrease in expression of mitochondrial genes and antioxidants, and decreased lysosomal biogenesis. Strikingly, the knockout mice were developmentally programmed as they showed an increased sensitivity to high-fat diet-induced obesity, hyperglycemia, hyperinsulinemia, increased adiposity, and cardiac remodeling. In summary, our results indicate a sexual dimorphism in placental autophagy in response to maternal obesity. We also show that autophagy plays an important role in placental function and that inhibition of placental autophagy programs the offspring to obesity, and to metabolic and cardiovascular diseases.

Indexed as

PlacentaSex CharacteristicsAnimalsAutophagyDiet, High-FatDisease Models, AnimalFemaleFetal DevelopmentHumansMice, KnockoutObesityPregnancyfetal programminghigh fat dietmaternal obesitymetabolomicsplacental functionsex differences

Identifiers

PMID26986453
PMCPMC4854539
OpenAlexW2314199535

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.