Mendeley  

Zotero  

Habibzadeh M, Hamedi S, Moeini A, Nasiri N, Hafezi M. Mesenchymal Stem Cell Therapy for Endometriosis: From Mechanistic Insights to Therapeutic Applications. ASWTR 2026; 23 (2) :26-37
URL: http://icml.ir/article-1-696-fa.html

Endometriosis is a chronic, estrogen-dependent inflammatory disorder affecting approximately 10–15% of women of reproductive age, characterized by the ectopic growth of endometrial-like tissue outside the uterine cavity. It is strongly associated with chronic pelvic pain, dysmenorrhea, infertility, and a marked decline in quality of life. Current therapeutic approaches, primarily hormonal therapy and surgery, remain largely symptomatic rather than curative, and are constrained by adverse effects, incomplete efficacy in many patients, and high recurrence rates. Consequently, there is a pressing need for disease-modifying, mechanistically targeted therapeutic strategies. Preclinical research has positioned mesenchymal stem cells (MSCs) as promising candidates for endometriosis treatment, owing to their immunomodulatory, anti-inflammatory, and regenerative capacities. This review synthesizes current mechanistic and preclinical evidence on MSC-based interventions. Experimental findings indicate that MSCs may modulate key pathogenic pathways—particularly NF-κB signaling and the COX-2/PGE2/E2 axis—thereby reducing inflammation, suppressing aberrant angiogenesis, and limiting fibrotic remodeling. Additional evidence suggests that MSCs support immune homeostasis by regulating both innate and adaptive immune responses and by promoting regulatory immune cell populations within the endometriotic microenvironment. The therapeutic benefits of MSCs appear to be mediated largely through paracrine mechanisms, involving the secretion of bioactive molecules, cytokines, growth factors, and extracellular vesicles such as exosomes. These factors are thought to contribute to tissue repair, immune modulation, and induction of apoptosis in ectopic endometrial cells. Nonetheless, preclinical results remain heterogeneous, varying by MSC source, experimental design, and disease model, and some studies report context-dependent pro-angiogenic effects. Despite this promise, clinical translation is hindered by cellular heterogeneity, safety concerns, and unresolved questions regarding optimal delivery route and dosing. As current evidence derives predominantly from in vitro and animal studies, with human data remaining scarce, MSC-based therapies for endometriosis should be regarded as experimental. Their safety and efficacy must be validated through well-designed clinical trials and standardized translational frameworks before adoption in routine clinical practice.