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The link between endometrial stromal cell senescence and decidualization in female fertility: the art of balance

  • Pavel Deryabin
  • Anastasiia Griukova
  • Nikolay Nikolsky
  • Aleksandra BorodkinaEmail author
Review

Abstract

Cell senescence seems to be an ambivalent biological phenomenon in many aspects. At the cellular level it is considered as an irreversible cell-cycle arrest commonly caused by the DNA damage. Senescent cells harbor a lot of impairments in various intracellular systems. Presence of senescent cells within tissues should ultimately lead to their malfunctioning. However, the interlink between cellular senescence and tissue/organismal functioning is far from always being unidirectional. The entangled and complex relationship between senescence and tissue-specific decidual differentiation of endometrial stromal cells (ESCs) is the excellent example reflecting dualism of cellular senescence. ESCs decidualization conditions endometrium responsiveness to embryonic signals and plays a critical role in embryo biosensoring, selection and implantation. Based on the analysis of the existing literary data, here we will try (1) to puzzle out how cellular senescence simultaneously may be an integral part of normal decidualization and may be involved in the progression of repeated implantation failures and recurrent pregnancy losses; (2) to suppose the sequence of cellular events reflecting the role of ESCs’ senescence during normal and impaired decidualization. Together, the deep scan of the interlink between ESCs’ senescence and decidualization will allow to suggest the preferable application scheme for senolytics targeting senescent cells as a possible approach to restore impaired endometrial receptivity and thus to increase the effectiveness of in vitro fertilization cycles.

Keywords

Mesenchymal stromal cells Cell aging Tissue-specific differentiation Reproduction 

Notes

Acknowledgements

The authors are thankful to Maria Sirotkina for the assistance in the figures design.

Funding

This study was funded by the Russian Science Foundation (# 19-74-10038).

Compliance with ethical standards

Conflict of interest

None declared.

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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of Intracellular Signaling and TransportInstitute of Cytology of the Russian Academy of SciencesSt-PetersburgRussia

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