Are matrix metalloproteinases and their inhibitors reliable diagnosis biomarkers and attractive therapeutic targets in endometriosis?

In: Metalloproteinases In Medicine · 2016 · vol. Volume 3 , pp. 81–92 · doi:10.2147/mnm.s102209 · W2560468099
article OA: diamond CC0 ⤵ 6 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-10

Matrix metalloproteinases and their inhibitors are present in endometriosis tissue, but inconsistent expression patterns limit their diagnostic utility, though rodent models support targeting them therapeutically.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-10

This review examines matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in endometriosis, summarizing literature on their expression in eutopic and ectopic endometrium and discussing whether reported changes are consistent enough to serve as diagnostic biomarkers or therapeutic targets. The authors highlight frequent controversies and difficulties in defining systematic, disease-associated differential regulation, and they further report reanalysis of publicly available whole-genome transcriptomic data showing occasional, unexplained eutopic overexpression of selective MMPs that undermines their reliability as diagnosis biomarkers; the review emphasizes that rodent model studies collectively support a role for MMPs in disease development and progression. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Abstract: Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are expressed in the human endometrium during the menstrual cycle, in particular to induce substantial extracellular matrix breakdown underlying menstruation. Endometriosis (EM) is characterized by the presence of endometrial tissue at ectopic locations. Because EM is thought to often develop from retrograde menstruation followed by implantation of menstrual tissue fragments at ectopic sites, endometrial MMPs and TIMPs were rapidly suspected as contributors to EM development and progression, generating hope for their use as biomarkers to facilitate EM diagnosis and as potential targets for developing new therapies against EM. Here, we not only summarize a substantial literature supporting the presence of MMPs and TIMPs in eutopic and ectopic endometrium of EM patients but also highlight frequent controversies on expression changes and the difficulty in identifying systematic MMP/TIMP differential regulation associated with the disease. Moreover, by reanalyzing publicly available data from a whole genome transcriptomic study, we show that occasional and unexplained endometrial overexpression of selective MMPs regardless of the disease and phase of the menstrual cycle rather discourages the use of eutopic MMPs and TIMPs as diagnosis biomarkers. However, we also review multiple studies using rodent models that collectively provide strong support to the contribution of MMPs in EM development and progression, and therefore to further investigations aiming at targeting MMP activity, especially in light of recent advances in new MMP inhibitors. Keywords: endometrium, endometriosis, biomarker, MMPs and TIMPs, therapy, animal model

My notes (saved in your browser only)

Condition tags

endometriosis

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.

References (100)

Cited by (6)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK