Protective role of stem cells in POI: Current status and mechanism of action, a review article

Sadeghi, Somaye; Mosaffa, Nariman; Huang, Boxian; Ramezani Tehrani, Fahimeh

doi:10.1016/j.heliyon.2023.e23271

Cited by 3 publications

(1 citation statement)

References 189 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Human mesenchymal stem cell therapy is a novel strategy for retain ovarian function and treat female infertility [ 17 ]. Available hMSCs include human bone marrow-derived mesenchymal stem cells, human adipose tissue-derived stem cells, and human amniotic membrane mesenchymal stem cells [ 18 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

Human mesenchymal stem cells derived exosomes improve ovarian function in chemotherapy-induced premature ovarian insufficiency mice by inhibiting ferroptosis through Nrf2/GPX4 pathway

Zhou,

Huang,

Zeng

et al. 2024

J Ovarian Res

View full text Add to dashboard Cite

Background Chemotherapy exposure has become a main cause of premature ovarian insufficiency (POI). This study aimed to evaluate the role and molecular mechanism of human umbilical cord mesenchymal stem cell-derived exosomes (hUMSC-Exos) in ovarian function protection after chemotherapy. Methods hUMSC-Exos were applied to cyclophosphamide-induced premature ovarian insufficiency mice and human ovarian granulosa tumor cells (KGN) to determine their effects on follicular development and granulosa cell apoptosis. Evaluation was done for iron ion and reactive oxygen species (ROS) production, lipid peroxidation levels, and changes in iron death-related molecules (nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Glutathione Peroxidase enzyme 4 (GPX4), and Solute carrier family 7 member 11 cystine glutamate transporter (SLC7A11; xCT)). Furthermore, rescue experiments using an Nrf2 inhibitor were performed to assess the therapeutic effects of hUMSC-Exos on granulosa cells. Results hUMSC-Exos promoted ovarian hormone levels and primary follicle development in POI mice and reduced granulosa cell apoptosis. After hUMSC-Exos treatment, the ROS production, free iron ions and lipid peroxidation levels of granulosa cells decreased, and the iron death marker proteins Nrf2, xCT and GPX4 also decreased. Furthermore, the Nrf2 inhibitor ML385 significantly attenuated the effects of hUMSC-Exos on granulosa cells. Conclusion hUMSC-Exos inhibit ferroptosis and protect against CTX-induced ovarian damage and granulosa cell apoptosis through the Nrf2/GPX4 signaling pathway, revealing a novel mechanism of hUMSC-Exos in POI therapy.

show abstract

Section: Discussionmentioning

confidence: 99%