| Authors | Homa Mollaei,, |
| Journal | Jentashapir Journal of Cellular and Molecular Biology |
| Page number | 164618-164625 |
| Serial number | 16 |
| Volume number | 4 |
| Paper Type | Full Paper |
| Published At | 2025 |
| Journal Type | Typographic |
| Journal Country | Iran, Islamic Republic Of |
| Journal Index | isc |
| Keywords | Uterine Fibroids, Cellular and Molecular Mechanisms, Genetic Mutations, MED, 12, HMGA2, TGF, β, Extracellular Matrix Remodeling |
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Abstract
Context: Uterine fibroids result from specific changes in the smooth muscle cells of the uterine wall. This condition typically
arises before menopause and during a woman's reproductive years and may be associated with heavy bleeding, pregnancy
complications, and pelvic pain. The major causes of uterine fibroid development include various environmental factors and
genetic mutations. These factors interact in complex ways that influence the initiation and progression of fibroids, affecting not
only cellular growth but also the extracellular matrix (ECM) remodeling within the uterus.
Evidence Acquisition: In this review study, to find relevant articles on the cellular and molecular mechanisms involved in the
development of uterine fibroids, published studies from 1995 onwards were searched on databases such as Google Scholar,
Scopus, PubMed, SID, and Magiran using keywords such as uterine fibroids, cellular and molecular mechanisms, and genetic
mutations. The selected studies were analyzed to provide a comprehensive overview of the most significant pathways and
genetic alterations that contribute to fibroid formation.
Results: Different cellular and molecular factors play a role in the formation of uterine fibroids, with the most important ones
being mutations in MED-12 and increased expression of HMGA2. Other genes involved in the growth and proliferation of uterine
fibroids include RAD51L1, COX6X, HEI10, ALDH2, RTVK-H3, and PCOLCE. Furthermore, the effects of multifunctional growth
factors such as TGF on increasing fibroid growth have been investigated. These findings emphasize the multifactorial nature of
fibroid development and highlight potential molecular targets for future therapeutic interventions.
Conclusions: Various methods have been proposed for the diagnosis, prevention, and treatment of uterine fibroids. However,
given the high prevalence of this condition and the complexity of its causative factors, a better understanding of the cellular
and molecular mechanisms involved can contribute to improving these methods. Ongoing research focusing on molecular
pathways may pave the way for more personalized and effective management strategies in the future.
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