Evidence map›Paper›PMID 36771423›Full record

ArticleNutrients2023

Adipocyte and Adipokines Promote a Uterine Leiomyoma Friendly Microenvironment.

Sadia Afrin, Malini Ramaiyer, Umme Aoufa Mafruha Begum, Mostafa A Borahay

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. A logistic regression model for predicting postoperative recurrence of cellular uterine leiomyoma.European journal of obstetrics & gynecology and reproductive biology: X · 2026
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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

4 authors.

Sadia AfrinDepartment of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-5063-9900
Malini RamaiyerSchool of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Umme Aoufa Mafruha BegumDepartment of Gynecology and Obstetrics, Khulna City Medical College Hospital, 25-26, KDA Ave., Khulna 9100, Bangladesh.
Mostafa A BorahayDepartment of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Funding

Mechanisms of actions(s) of simvastatin in uterine leiomyomaR01HD094380 · NICHD · JOHNS HOPKINS UNIVERSITY · PI BORAHAY, MOSTAFA A. · 2018 to 2022
$4.0M
Eunice Kennedy Shriver National Institute of Child Health and Human Development R01HD094380
6 · The paper itself

Abstract

Uterine leiomyomas are the most common benign tumors of the female reproductive system. Obese individuals have a higher burden of uterine leiomyoma, yet the mechanism relating obesity and leiomyoma development remains unknown. In this study, we observe the effect of adipocyte coculture and leptin treatment on human myometrium and leiomyoma cells. We isolated primary leiomyoma and myometrium cells from hysterectomy or myomectomy patients. Protein expression levels of phosphorylated ERK1/2/total ERK1/2, phosphorylated STAT3/total STAT3, and phosphorylated AKT1/2/3/total AKT1/2/3 were quantified using immunoblotting in immortalized and primary leiomyoma and myometrial cells cocultured with human adipocytes and treated with leptin. An enzyme-linked immunosorbent assay (ELISA) was used to assess pro-inflammatory, fibrotic, and angiogenic factors in immortalized human myometrium and leiomyoma cells treated with leptin. The effects of STAT3, ERK, and AKT inhibitors were assessed in leiomyoma cell lines additionally cultured with adipocytes. Adipocyte coculture and leptin treatment increases the expression of JAK2/STAT3, MAPK/ERK, and PI3K/AKT signaling while inhibitors suppressed this effect. Leptin induces a tumor-friendly microenvironment through upregulation of pro-inflammatory (IFNγ, IL-8, IL-6, GM-CSF, MCP-1, and TNF-α), fibrotic (TGF-β1, TGF-β2, and TGF-β3), and angiogenic (VEGF-A, HGF, and Follistatin) factors in human leiomyoma cells. Furthermore, adipocyte coculture and leptin treatment increases leiomyoma cells growth through activation of MAPK/ERK, JAK2/STAT3, and PI3k/AKT signaling pathways. Finally, STAT3, ERK, and AKT inhibitor treatment suppressed PCNA, TNF-α, TGF-β3, and VEGF-A intracellular staining intensity in both adipocyte coculture and leptin treated leiomyoma cells. These findings suggest that, in obese women, adipocyte secreted hormone or adipocytes may contribute to leiomyoma development and growth by activating leptin receptor signaling pathways.

Indexed as

LeiomyomaUterine NeoplasmsAdipocytesAdipokinesFemaleHumansLeptinObesityPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTransforming Growth Factor beta3Tumor MicroenvironmentTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AAdipokinesLeptinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTransforming Growth Factor beta3Tumor Necrosis Factor-alphaVascular Endothelial Growth Factor AadipocyteJAK2/STAT3leiomyomaleptinMAPK/ERKPI3K/AKT

Identifiers

PMID36771423
PMCPMC9919329

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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.