Endometriosis is a significant disease characterized by
infertility and
pelvic pain in which endometrial stromal and glandular tissue grow in ectopic locations. Altered responsiveness to
progesterone is a contributing factor to
endometriosis pathophysiology, but the precise mechanisms are poorly understood. Progesterone resistance influences both the eutopic and ectopic (endometriotic lesion) endometrium. An inability of the eutopic endometrium to properly respond to
progesterone is believed to contribute to the
infertility associated with the disease, while an altered responsiveness of endometriotic lesion tissue may contribute to the survival of the
ectopic tissue and associated symptoms. Women with
endometriosis express altered levels of several endometrial
progesterone target genes which may be due to the abnormal expression and/or function of
progesterone receptors and/or chaperone
proteins, as well as
inflammation, genetics, and epigenetics.
MiRNAs are a class of epigenetic modulators proposed to play a role in
endometriosis pathophysiology, including the modulation of
progesterone signaling. In this paper, we summarize the role of
progesterone receptors and
progesterone signaling in
endometriosis pathophysiology, review
miRNAs, which are over-expressed in
endometriosis tissues and fluids, and follow this with a discussion on the potential regulation of key
progesterone signaling components by these
miRNAs, concluding with suggestions for future research endeavors in this area.