Targeting NGF but not VEGFR1 or BDNF signaling reduces endometriosis-associated pain in mice.

ABSTRACT:

Introduction

Endometriosis is a chronic inflammatory disease that affects ∼10 % of women. A significant fraction of patients experience limited or no efficacy with current therapies. Tissue adjacent to endometriosis lesions often exhibits increased neurite and vascular density, suggesting that disease pathology involves neurotrophic activity and angiogenesis.

Objectives

We aim to evaluate the potential for key tyrosine-kinase-receptor-coupled neurotrophic molecules to contribute to endometriosis-associated pain in mice.

Methods

Peritoneal fluid was collected from endometriosis patients undergoing surgery and the levels of NGF and VEGFR1 regulators (VEGFA, VEGFB, PLGF, and sVEGFR1) were quantified by ELISA. VEGFR1 regulator concentrations were used to calculate VEGFR1

SUBMITTER: Zaninelli TH 

PROVIDER: S-EPMC12225929 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature