Causal analysis of the development of uterine adenomyosis in mice
article
OA: closed
CC0
⤵ 7 in-corpus citations
Limited metadata. Only one source feed has indexed
this record so far — no abstract, full text, or open-access copy is
available through Endo Lab. The
publisher
is the canonical location for the actual content. If you have institutional
access, use "Find at my library".
AI-generated summary
This study investigated the causal mechanisms underlying the development of uterine adenomyosis in a mouse model, focusing on key cellular and molecular events.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
My notes (saved in your browser only)
Condition tags
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.
Cited by (7)
- Magnetic Resonance Imaging-guided Focused Ultrasound Surgery in a Swine Adenomyosis Model 2023
- Increase in the number of integrinβ1-immunoreactive monocyte-lineage cells in experimentally-induced adenomyosis in mice 2003
- Suppression of the Development of Experimentally Induced Uterine Adenomyosis by a Novel Matrix Metalloproteinase Inhibitor, ONO-4817, in Mice 2001
- Changes in Uterine Microvessels as a Possible Pathogenic Factor in the Development of Adenomyosis Induced by Pituitary Grafting in Mice. 1999
- Increased expression of prolactin receptor mRNA in adenomyotic uterus in mice 1997
- Disturbed Cell Arrangement, Increased Cell Membrane Permeability and Apoptotic Cell Death Occur in Adenomyotic Uterine Tissues in Mice 1997
- Animal model of uterine adenomyosis: Is prolactin a potent inducer of adenomyosis in mice? 1991
Source provenance
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0
· commercial use OK