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. 2023 Nov 13;14:327. doi: 10.1186/s13287-023-03551-w

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Autologous transplantation of MenSCs for improving chemotherapy-induced POI. Firstly, isolation of MenSCs from patients menstrual blood or endometrial tissue before receiving chemotherapy. After culture and amplification in vitro, MenSCs was cryopreserved in liquid nitrogen for further application. Subsequently, once the patient received chemotherapy, the chemotherapeutic drugs can cause ovarian toxicity mainly through impairing stromal tissue, oocytes, granulosa cells, and blood vessels, as well as aggravating oxidative stress which plays an important role in ovarian injury. Thirdly, after chemotherapy ends, the pre-cryopreserved autologous MenSCs can be transfused into the patient through intravenous injection, arterial intervention, and ovarian injection under laparoscopy. Finally, the transplanted MenSCs repair the ovarian dysfunction through enhancing the anti-apoptotic capacity of ovarian cells, preventing ovarian follicular atresia, promoting angiogenesis and improving injured ovarian structure. And these improvements are mainly attributed to MenSC-derived biological factors, functional RNAs, and even mitochondria, which are directly secreted or indirectly translocated with extracellular vesicles (microvesicles and exosomes) to repair ovarian dysfunction. The schematic diagram is created with BioRender.com