Background: Endometriosis remains a challenging condition for clinicians to treat. To improve
our results, we have to develop new treatment strategies based on pathophysiological mechanisms
targeting the etiologic and pathogenic processes involved.
Objectives: Revise new inflammatory pathogenic mechanisms involved in endometriosis, namely inflammasome.
Method: Literature review for the updating of data to give new clues for different options of treatments.
Results: Inflammasome has been described as a multiprotein complex and is considered a key regulator
of the innate and adaptive host response that surveys the cytosol and other compartments into the cell. It
is involved in the immediate detection and responds to the presence of danger- and pathogen-associated
molecular patterns named DAMPs and PAMPs respectively, and has been described in several cells,
mainly on immune cells of the myeloid lineage and epithelial cells in tissues with mucosal surfaces. Four
inflammasome are formed in a stimulus-dependent manner of distinct composition. They are the Noll
Like Receptors (NLR) proteins Nlrp1b, Nlrp3, Nlrc4, and Nlrp6, as well as the absent in melanoma 2
(AIM2). They activate the production of IL-1β and IL-18 that induce a host response such as pyroptosis,
a proinflammatory cell death and the secretion of leaderless cytokines and growth factors. Inflammasome
is linked to atherosclerosis, periodic fever syndromes, vitiligo, Crohn’s disease, gout, asbestosis,
silicosis, Alzheimer’s disease and periodontitis. Endometriosis has been related with IL-1β and Another
NLR, Nlrp7, was correlated with myometrial invasion in human endometrial cancer tissue.
Conclusions: These new clues regarding the pathogenic mechanisms involving the inflammasome
may be crucial in the future development for endometriosis therapy.