Inflammasome as a Key Pathogenic Mechanism in Endometriosis

Pedro Bullon, Pedro Bullón, Jose Manuel Navarro, José Manuel Navarro, Navarro JM
Current drug targets · 2017 · vol. 18(9) , pp. 997–1002 · doi:10.2174/1389450117666160709013850 · PMID:27397068 · W2490159889
article OA: closed CC0 ⤵ 40 in-corpus citations
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This review examines the inflammasome, a multiprotein complex involved in host defense, as a key pathogenic mechanism in endometriosis, potentially offering new therapeutic targets.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-09 · read from full text ⓘ

This paper reviews existing evidence on inflammasome-related inflammatory pathogenic mechanisms in endometriosis, focusing on how inflammasome complexes detect DAMPs and PAMPs and drive host responses. It summarizes that four stimulus-dependent inflammasome types (NLR proteins Nlrp1b, Nlrp3, Nlrc4, Nlrp6, and AIM2) activate IL-1β and IL-18, which can promote pyroptosis and secretion of proinflammatory mediators. The paper also notes inflammasome has been linked to multiple diseases, and it specifically states that endometriosis has been related with IL-1β, while another NLR (Nlrp7) was correlated with myometrial invasion in human endometrial cancer tissue. As a literature review, it updates and integrates prior data rather than presenting new experimental results, and it does not provide detailed methodological limitations beyond its scope as an updating review. This paper is centrally about endometriosis—specifically, it focuses on inflammasome-driven innate immune inflammation mechanisms potentially relevant to endometriosis pathogenesis.

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Abstract

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.
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Abstract

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.

Keywords

Molecular, pathways, inflammation, NLRP-3, DAMP, PAMP. 144 17

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammasomes Endometriosis Endometriosis Female Humans Inflammasomes Inflammasomes

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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