Prof. L. Griffith (MIT) receives NIH award to advance research into gynecological diseases using microphysiological systems

18 March 2026

Linda Griffith, Professor of Biological Engineering and Mechanical Engineering at Massachusetts Institute of Technology (MIT), where she also directs the Center for Gynepathology Research, has been awarded a $3M per year NIH grant to establish a new Technology Development Center.

This amount was earmarked as part of NIH Complement ARIE program that has pledged over

$150M to developing and scaling new approach methods in biomedical research that better simulate human biology than animal models.

Building on Griffith’s work in endometriosis, a debilitating gynecological disorder affecting about 10% of women and girls, the Center will establish next gen microphysiological systems to advance research into diseases of the female reproductive tract. In a field where financial support has consistently lagged behind medical need, this grant carries particular importance.

Owing to human-specific features of the menstrual cycle, hormonal regulation, and immune system, the most commonly used model organisms, such as rodents, are not adequate for modeling endometriosis. The absence of human‑relevant models has so far hindered the ability of researchers to investigate the mechanisms driving the disease, contributing to slow scientific progress and leaving many patients with persistent pain and chronic inflammation.

The in vitro models that incorporate perfusable microvasculature, capturing endothelial-fibroblast-epithelial interactions and enabling immune cell trafficking, are particlarly well-suited for analyzing patient-specific disease features and responses to therapies.

Griffith’s work on building the endometriosis patient lesions in organs-on-a-chip will allow to better understand the molecular and cellular underpinnings of the disease, identify new therapeutic targets and assess treatment efficacy.

Griffith's team May 2026 publication notably describes how mixing endothelial cells with supporting cells in a synthetic-extracellular matrix precursor solution, before seeding into the central channel of a microfluidic device and introducing continous fluid flow, allowed to obtain pefusable microvessels that captured the architectural features of native blood vessels. The co-culture of these microvessels with human endometrial epithelial patient-derived organoids and macrophages formed the foundation for modeling endometriosis in vitro, supporting future drug testing studies.

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