- Asherman’s syndrome is a rare disease characterized by intrauterine scars that causes infertility and menstrual abnormalities
- This study describes the cellular alterations responsible for Asherman’s syndrome at the single-cell level for the first time
The study ‘Decoding the endometrial niche of Asherman’s Syndrome at single-cell resolution’, published by Dr. Carlos Simon and his research team (University of Valencia, INCLIVA and Carlos Simon Foundation) in the scientific journal Nature Communications, describes the cellular alterations responsible for Asherman’s Syndrome at the single-cell level for the first time. This new study also identifies the gene expression profiles that create a dysfunctional uterine environment, promoting scar tissue formation, inflammation, and a reduction in the development of new blood vessels
About the study
This study recruited patients diagnosed with moderate or severe Asherman’s syndrome, fertile women, and healthy donors as control groups
More than 200,000 cells from the endometrium of patients with Asherman’s syndrome and healthy, fertile patients were analyzed. By incorporating cutting-edge machine learning models, the research team compared transcriptomic profiles from in vivo and in vitro endometrial cells, providing further insight into the disease-associated alterations to the endometrial microenvironment
These patients are part of an ongoing clinical study, currently in phase I/II, seeking to validate the effects of therapy with the patient’s own bone marrow-derived stem cells (CD133+) on their clinical reproductive outcomes
The study also created endometrial organoids from affected patients and healthy women. Organoids – miniaturized endometrial organs generated in the laboratory – displayed similar responses to endometrial tissue in vivo, suggesting organoids as a robust in vitro model to study Asherman’s syndrome
Article reference
Santamaria, X., Roson, B., Perez-Moraga, R. et al. Decoding the endometrial niche of Asherman’s Syndrome at single-cell resolution. Nat Commun 14, 5890 (2023). https://doi.org/10.1038/s41467-023-41656-1