CV


FA
Homa Mollaei

Homa Mollaei

Assistant Professor

Faculty: Science

Degree: Ph.D

CV
FA
Homa Mollaei

Assistant Professor Homa Mollaei

Faculty: Science Degree: Ph.D |

A Review of Cellular and Molecular Mechanisms Involved in the Development of Uterine Fibroids

AuthorsHoma Mollaei,,
JournalJentashapir Journal of Cellular and Molecular Biology
Page number164618-164625
Serial number16
Volume number4
Paper TypeFull Paper
Published At2025
Journal TypeTypographic
Journal CountryIran, Islamic Republic Of
Journal Indexisc
KeywordsUterine Fibroids, Cellular and Molecular Mechanisms, Genetic Mutations, MED, 12, HMGA2, TGF, β, Extracellular Matrix Remodeling

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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