Evidence map›Paper›PMID 37843712›Full record

ArticleMolecular biology reports2023

Myricetin attenuates hypoxia-induced inflammation in human adipocytes.

Kathrin Geiger, Axel Muendlein, Andreas Leiherer, Stella Gaenger, Eva Maria Brandtner, Martin Wabitsch, Peter Fraunberger, Heinz Drexel, Christine Heinzle

Abstract read
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In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

9 authors at 2 institutions in 3 countries.

Kathrin GeigerVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria. kathrin.geiger@vivit.at.ORCID http://orcid.org/0009-0005-1623-3938
Axel MuendleinVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Andreas LeihererVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Stella GaengerVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Eva Maria BrandtnerVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Martin WabitschDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Peter FraunbergerMedical Central Laboratories, Feldkirch, Austria.
Heinz DrexelVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Christine HeinzleVorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.
Vorarlberg Institute for Vascular Investigation and Treatment · ATPrivate University in the Principality of Liechtenstein · LI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdipose tissue hypoxia plays a crucial role in the development of chronic low-grade systemic inflammation which has been associated with the pathogenesis of obesity-related diseases. Myricetin is a natural compound present in numerous plant-based foods with presumed anti-inflammatory and beneficial health effects. The impact of this flavonoid on hypoxia-induced expression of inflammatory adipokines and hypoxia-regulated pathways is unknown so far and has been addressed in the present study.

methodsDifferentiated human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were cultured with or without myricetin under normoxic and hypoxic conditions for varying time periods. The effect of hypoxia and myricetin on the expression of the investigated adipokines was measured by real-time RT-PCR. Western blot analysis was used for the detection of transcription factors involved in hypoxia-regulated pathways.

resultsMyricetin interfered in the hypoxia-induced regulation of adipokines and the underlying pathways, which are involved in transmitting the inflammatory response. It strongly repressed hypoxia-induced expression of apelin, leptin, chemerin, asprosin, and DPP-4 and HIF-1α accumulation in the nucleus was diminished. Furthermore, the activation of the key regulators in the inflammatory response NF-κB, Akt, and CREB was suppressed by myricetin under hypoxic conditions. Myricetin also decreased hypoxia-induced accumulation of the pro-tumorigenic transcription factors Snail and Slug in the nucleus.

conclusionTaken together, our results indicated that myricetin regulated hypoxia-induced expression of adipokines and hypoxia-regulated pathways in human adipocytes. Our study therefore provided evidence of the anti-inflammatory effects of myricetin in hypoxia-treated human adipocytes.

Indexed as

AdipocytesHypoxiaAdipokinesAnti-Inflammatory AgentsArrhythmias, CardiacCell HypoxiaFlavonoidsGenetic Diseases, X-LinkedGigantismHeart Defects, CongenitalHumansHypoxia-Inducible Factor 1, alpha SubunitInflammationIntellectual DisabilityAdipokinesAnti-Inflammatory AgentsFlavonoidsHypoxia-Inducible Factor 1, alpha SubunitmyricetinAdipokinesHIF-1αHypoxiaMyricetinNF-κBSGBS adipocytes

Identifiers

PMID37843712
OpenAlexW4387660947

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Registered trials

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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.