Evidence map›Paper›PMID 32208164›Full record

ArticleRedox biology2020

Low steady-state oxidative stress inhibits adipogenesis by altering mitochondrial dynamics and decreasing cellular respiration.

Raquel Fernando, Kristina Wardelmann, Stefanie Deubel, Richard Kehm, Tobias Jung, Marco Mariotti, Aphrodite Vasilaki, Vadim N Gladyshev, André Kleinridders, Tilman Grune and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 31 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

11 authors at 7 institutions in 3 countries.

Raquel FernandoDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany.
Kristina WardelmannGerman Center for Diabetes Research (DZD), 85764, München-Neuherberg, Germany; Central Regulation of Metabolism Group, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany.
Stefanie DeubelDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany.
Richard KehmDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764, München-Neuherberg, Germany.
Tobias JungDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany.
Marco MariottiDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Aphrodite VasilakiMRC-Arthritis Research UK Centre for Integrated Research Into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, UK.
Vadim N GladyshevDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
André KleinriddersGerman Center for Diabetes Research (DZD), 85764, München-Neuherberg, Germany; Central Regulation of Metabolism Group, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany.
Tilman GruneDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764, München-Neuherberg, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Berlin, Germany.
José Pedro CastroDepartment of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbrücke, 14558, Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764, München-Neuherberg, Germany; Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA. Electronic address: jquintaaraujocastro@bwh.harvard.edu.
German Institute of Human Nutrition · DEHarvard University · USBrigham and Women's Hospital · USDeutsches Diabetes-Zentrum e.V. · DEGerman Center for Diabetes Research · DEHeinrich Heine University Düsseldorf · DEUniversity of Liverpool · GB

Funding

Medical Research Council MR/P020941/1
6 · The paper itself

Abstract

Adipogenesis is a fundamental process of white adipose tissue function, supporting lipid storage and release, while avoiding its spillover and ectopic accumulation in tissues and organs. During aging adipogenesis is impaired and among other factors, oxidative stress contributes to this process. Adipogenesis requires functional and dynamic mitochondria; however, this organelle itself becomes dysfunctional during aging and accounts for most of reactive oxygen species (ROS) production. Here, we evaluated whether oxidative stress impairs adipogenesis through functional impairment of mitodynamics by utilizing hyperoxia as a continuous source of oxidative stress while maintaining cellular viability. This negatively impacted mitochondrial function, including respiration and dynamics and ultimately blocked adipogenesis. Interestingly, this state was reversible by using the antidiabetic drug, Rosiglitazone, which reduced oxidative stress, restored mitochondrial dynamics and respiration and augmented adipogenesis. Moreover, in vitro results were in agreement with in vivo models of oxidative stress and aging, in which mice depleted of the superoxide dismutase enzyme 1 (SOD1) and old wild-type C57BL/6JRj mice demonstrated the same trend of adipogenic potential. Importantly, in humans the results follow the same pattern, showing a downregulation of adipogenic markers during aging. Since the levels of oxidative stress and peripheral insulin resistance increase with age, while adipogenesis decreases during aging, our model helps to understand a possible way to overcome physiologically low, steady stress conditions and restore adipogenesis, avoiding accumulation of deleterious hypertrophic adipocytes in favor of beneficial hyperplasia.

Indexed as

AdipogenesisMitochondrial DynamicsAnimalsCell RespirationMiceMice, Inbred C57BLOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesAdipogenesisHyperoxiaMitochondrial dysfunctionOxidative stressRosiglitazone

Identifiers

PMID32208164
PMCPMC7097524
OpenAlexW3012448001

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.