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Related Experiment Video

Updated: Jul 6, 2026

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens

Published on: May 23, 2014

Targeting Cellular Senescence to Enhance Human Endometrial Stromal Cell Decidualization and Inhibit Their Migration.

Julia Delenko^1,2,3, Nathaniel Hyman^1,2, Prodyot K Chatterjee^1,2

¹Northwell, 2000 Marcus Ave, Suite 300, New Hyde Park, NY 11042, USA.

|June 26, 2025

Summary

Flavonoid senolytics like quercetin effectively improve uterine receptivity by clearing senescent cells. These compounds show promise for treating endometriosis and infertility, offering a new therapeutic avenue.

Keywords:

endometriosis flavonoids infertility menstrual effluent quercetin senescence senolytic senomorphic

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Last Updated: Jul 6, 2026

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens

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Published on: May 23, 2014

Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization

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Published on: March 2, 2017

Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization

Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization

Published on: September 1, 2018

Area of Science:

Reproductive Biology
Cellular Biology
Pharmacology

Background:

Cellular senescence, characterized by cell cycle arrest and inflammation, contributes to various health issues.
Senescent endometrial stromal cells (eSCs) are implicated in endometriosis and infertility by impairing decidualization, crucial for uterine receptivity.
Senotherapeutics, including senolytics and senomorphics, are being developed to target cellular senescence.

Purpose of the Study:

To compare the effects of various senotherapeutics on senescent endometrial stromal cells (eSCs) relevant to endometriosis.
To identify optimal senotherapeutic compounds for potential clinical application in endometriosis and infertility.

Main Methods:

Utilized menstrual effluent-derived eSCs to assess senotherapeutic efficacy.
Evaluated flavonoid and non-flavonoid compounds for their impact on eSC function, decidualization, migration, and cytotoxicity.
Investigated mechanistic pathways including AKT and p53 phosphorylation, and ERK1/2 phosphorylation.

Main Results:

Flavonoid senolytics (quercetin, fisetin, luteolin) and kaempferol significantly improved decidualization without cytotoxicity.
Dasatinib enhanced decidualization, while other non-flavonoids showed cytotoxicity.
Flavonoids and dasatinib inhibited eSC migration, suppressed AKT phosphorylation, upregulated p53, and eliminated senescent eSCs. Quercetin and fisetin also reduced ERK1/2 phosphorylation.

Conclusions:

Flavonoid senolytics and dasatinib demonstrate significant potential in improving eSC function and reducing senescence.
Flavonoid senolytics, particularly quercetin and fisetin, are promising candidates for further in vivo studies to treat endometriosis and infertility.