Evidence map›Paper›PMID 31445519›Full record

ArticleReproductive biology and endocrinology : RB&E2019

Endometrium and endometriosis tissue mitochondrial energy metabolism in a nonhuman primate model.

Hannah M Atkins, Manish S Bharadwaj, Anderson O'Brien Cox, Cristina M Furdui, Susan E Appt, David L Caudell

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Hannah M AtkinsDepartment of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, One Medical Center Blvd, Winston-Salem, NC, 27157, USA.
Manish S BharadwajAgilent Technologies, Cell Analysis Division, Lexington, MA, USA.
Anderson O'Brien CoxDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Cristina M FurduiDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Susan E ApptDepartment of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, One Medical Center Blvd, Winston-Salem, NC, 27157, USA.
David L CaudellDepartment of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, One Medical Center Blvd, Winston-Salem, NC, 27157, USA. dcaudell@wakehealth.edu.
Wake Forest University · USAgilent Technologies (United States) · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Wake Forest Clinical and Translational Science AwardUL1TR001420 · NCATS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ARD, JAMY D, FOLEY, KRISTIE L · 2015 to 2023
$32.3M
Dietary Mitigation of Psychosocial Stress Effects on CVD Risk R01HL087103 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SHIVELY, CAROL A. · 2007 to 2017
$6.0M
Laboratory Animal & Comparative Medicine TrainingT32OD010957 · OD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI J. MARK CLINE · 2012 to 2026
$4.3M
Department of Pathology-Comparative Medicine Internal Pilot Award 125-120310-00000-830086National Institutes of Health (US) P30CA012197NCATS NIH HHS UL1 TR001420NCI NIH HHS P30 CA012197NHLBI NIH HHS R01 HL087103NIH HHS R01HL087103NIH HHS T32 OD010957NIH HHS UL1TR001420NIH Office of the Director T32OD010957-37
6 · The paper itself

Abstract

backgroundEndometriosis is the growth of uterine lining (endometrium) outside of the uterus. In other chronic inflammatory diseases, mitochondrial dysfunction is suspected of playing a role in disease pathogenesis. However, little is known about endometriosis mitochondrial function or its effects on tissue metabolism. The objectives of this study were to analyze mitochondrial function in nonhuman primate (NHP) endometrium and endometriosis tissue and to identify the metabolic features of these tissues that may contribute to disease.

methodsMitochondrial function in endometriosis tissue and endometrium was measured using mitochondrial respirometry analysis to determine if changes in oxidative phosphorylation exist in endometrium and endometriosis tissue compared to control endometrium from clinically healthy NHPs. Targeted metabolomics and multidimensional statistical analysis were applied to quantify key metabolites in energy and amino acid biosynthesis pathways.

resultsMitochondrial respirometry assays showed endometrium from NHPs with endometriosis had reduced complex II-mediated oxygen consumption rates (OCR) across all energy states (basal, p = 0.01; state 3, p = 0.02; state 3u, p = 0.04; state 4o, p = 0.008) and endometriosis tissue had reduced state 3, complex I-mediated OCR (p = 0.02) and respiratory control rates (p = 0.01) compared to normal endometrium. Targeted metabolomics performed on tissue revealed carnitine (p = 0.001), creatine phosphate (p = 0.01), NADH (p = 0.0001), FAD (p = 0.001), tryptophan (p = 0.0009), and malic acid (p = 0.005) were decreased in endometriosis tissue compared to normal endometrium samples. FAD (p = 0.004), tryptophan (p = 0.0004) and malic acid (p = 0.03) were significantly decreased in endometrium from NHPs with endometriosis compared to normal endometrium. Significant metabolites identified in endometriosis and endometrium samples from animals with endometriosis were part of amino acid biosynthesis or energy metabolism pathways.

conclusionsHere, endometrial mitochondrial energy production and metabolism were decreased in endometrium and endometriosis tissue. Decreased mitochondrial energy production may be due to oxidative stress-induced damage to mitochondrial DNA or membranes, a shift in cell metabolism, or decreased energy substrate; however, the exact cause remains unknown. Additional research is needed to determine the implications of reduced mitochondrial energy production and metabolism on endometriosis and endometrium.

Indexed as

Energy MetabolismAnimalsElectron Transport Chain Complex ProteinsEndometriosisEndometriumFemaleHumansMacaca fascicularisMacaca mulattaMitochondriaPrimatesSpecies SpecificityElectron Transport Chain Complex ProteinsEndometriosisInfertilityMetabolismMitochondrial functionNonhuman primate

Identifiers

PMID31445519
PMCPMC6708555
OpenAlexW2969948750

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.