Evidence map›Paper›PMID 38168580›Full record

ArticleScientific reports2024

Quercetin stimulates trophoblast fusion via the mitochondrial function.

Kanoko Yoshida, Kazuya Kusama, Go Shinohara, Shiho Sato, Mikihiro Yoshie, Kazuhiro Tamura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Quercetin ReducesInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Protective Role of Rosmarinic Acid-EnrichedBiochemistry research international · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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

6 authors at 1 institution in 1 country.

Kanoko YoshidaDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Kazuya KusamaDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan. kusamak@toyaku.ac.jp.
Go ShinoharaDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Shiho SatoDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Mikihiro YoshieDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Kazuhiro TamuraDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Tokyo University of Pharmacy and Life Sciences · JP

Funding

Japan Society for the Promotion of Science 20H03133
6 · The paper itself

Abstract

The fusion of mononuclear trophoblasts into multinucleate syncytiotrophoblasts is the critical event in the process of syncytialization, and its dysregulation can lead to pregnancy complications, notably hypertensive disorders of pregnancy (HDP). Oxidative stress may disrupt trophoblast syncytialization in HDP. Specifically, placentas with HDP exhibit impaired mitochondria, giving rise to the generation of reactive oxygen species (ROS) and subsequent oxidative stress. Quercetin, a bioflavonoid known for its antioxidant and anti-aging properties, has the potential to mitigate oxidative stress during trophoblast syncytialization. However, the precise mechanism underlying the action of quercetin in these processes remains to be elucidated. To explore the impact of quercetin on syncytialization, mitochondrial function, and ROS generation, cyclic AMP-stimulated BeWo cells were treated with quercetin. The expression of markers associated with cell fusion, mitochondrial function, and oxidative stress was determined using qPCR and western blotting. Additionally, morphological syncytialization and mitophagy (mitochondrial degradation) were assessed by immunofluorescence analysis. Our results revealed that quercetin increased the expression of syncytialization markers and promoted cell fusion. Furthermore, this compound also upregulated markers associated with mitophagy and mitochondrial fusion, which are corroborated by visual evidence of mitophagy through the fluorescence microscope. Cell fusion naturally stimulated ROS generation, which was attenuated by quercetin. Quercetin downregulated the expression of NRF2 and HO-1 during syncytialization, while increasing the expression of sirtuin1/3/6, which are known to play essential roles in antioxidant responses. In conclusion, quercetin effectively regulates mitochondrial function through its antioxidant properties and the suppression of ROS generation, ultimately promoting trophoblast fusion, suggesting that the flavonoid has the potential to ameliorate pregnancy-related disorder stemming from placental dysplasia.

Indexed as

PlacentaQuercetinAntioxidantsFemaleHumansMitochondriaPregnancyReactive Oxygen SpeciesTrophoblastsAntioxidantsQuercetinReactive Oxygen Species

Identifiers

PMID38168580
PMCPMC10762005
OpenAlexW4390496561

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.