Ovarian hormones-autophagy-immunity axis in menstruation and endometriosis

Theranostics. 2021 Jan 19;11(7):3512-3526. doi: 10.7150/thno.55241. eCollection 2021.

Abstract

Menstruation occurs in few species and involves a cyclic process of proliferation, breakdown and regeneration under the control of ovarian hormones. Knowledge of normal endometrial physiology, as it pertains to the regulation of menstruation, is essential to understand disorders of menstruation. Accumulating evidence indicates that autophagy in the endometrium, under the regulation of ovarian hormones, can result in the infiltration of immune cells, which plays an indispensable role in the endometrium shedding, tissue repair and prevention of infections during menstruation. In addition, abnormal autophagy levels, together with resulting dysregulated immune system function, are associated with the pathogenesis and progression of endometriosis. Considering its potential value of autophagy as a target for the treatment of menstrual-related and endometrium-related disorders, we review the activity and function of autophagy during menstrual cycles. The role of the estrogen/progesterone-autophagy-immunity axis in endometriosis are also discussed.

Keywords: NK cell; autophagy; endometrium; estrogen; macrophage; menstruation; neutrophil; progesterone.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adult
  • Autophagosomes / genetics
  • Autophagosomes / immunology
  • Autophagy / drug effects
  • Autophagy / genetics
  • Autophagy / immunology*
  • Endometriosis / etiology
  • Endometriosis / genetics
  • Endometriosis / immunology*
  • Endometriosis / pathology
  • Endometrium / cytology
  • Endometrium / drug effects
  • Endometrium / immunology*
  • Epithelial Cells / cytology
  • Epithelial Cells / drug effects
  • Epithelial Cells / immunology
  • Estrogens / immunology
  • Estrogens / metabolism
  • Estrogens / pharmacology*
  • Female
  • Gene Expression Regulation
  • Humans
  • Killer Cells, Natural / cytology
  • Killer Cells, Natural / drug effects
  • Killer Cells, Natural / immunology
  • MAP Kinase Signaling System / genetics
  • MAP Kinase Signaling System / immunology
  • Macrophages / cytology
  • Macrophages / drug effects
  • Macrophages / immunology
  • Menstruation / immunology*
  • Neutrophils / cytology
  • Neutrophils / drug effects
  • Neutrophils / immunology
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / immunology
  • Progesterone / immunology
  • Progesterone / metabolism
  • Progesterone / pharmacology*
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / immunology

Substances

  • Estrogens
  • Progesterone
  • Proto-Oncogene Proteins c-akt