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Mouse Knockout Models for Pelvic Organ Prolapse: a Systematic Review
Kristina Allen-Brady1, Maria A T Bortolini2, Margot S Damaser3,4,5
1Department of Internal Medicine, University of Utah, Williams Building 295 Chipeta Way, Salt Lake City, UT, USA. kristina.allen@utah.edu.
International Urogynecology Journal
|January 28, 2022
Summary
Mouse knockout models reveal connective tissue defects in pelvic organ prolapse (POP). Loxl1 and Fbln5 models are key for understanding POP pathophysiology and potential treatments.
Area of Science:
- Reproductive biology
- Genetics
- Connective tissue disorders
Background:
- Pelvic organ prolapse (POP) is linked to connective tissue defects and impaired elastic matrix remodeling.
- Mouse knockout (KO) models offer insights into POP pathogenesis.
Purpose of the Study:
- To summarize available mouse KO models for POP.
- To elucidate pathophysiological mechanisms of POP development using these models.
Main Methods:
- Systematic review following PRISMA guidelines.
- Searched PubMed, Scopus, and Embase (2000-2021).
- Included 25 articles and 11 conference abstracts.
Main Results:
- Five KO models studied: Loxl1, Fbln5, Fbln3, Hoxa11, Upii-sv40t.
- Loxl1 and Fbln5 KO models show reliable POP phenotypes.
- Loxl1 KO mice exhibit POP post-partum; Fbln5 KO mice develop POP with aging.
Conclusions:
- Mouse KO models are valuable for studying POP development and progression.
- These models aid in investigating POP treatments and mesh complications.
