Mechanical Signaling and Extracellular Matrix in Uterine Fibroids
| Autor: | Saima Rafique, Phyllis C. Leppert, James H. Segars |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Uterine fibroids Endocrinology Diabetes and Metabolism Apoptosis Mechanotransduction Cellular Models Biological Extracellular matrix 03 medical and health sciences 0302 clinical medicine Endocrinology Fibrosis Leiomyomatosis Physiology (medical) Internal medicine medicine Humans Mechanotransduction chemistry.chemical_classification 030219 obstetrics & reproductive medicine Leiomyoma Chemistry Therapies Investigational Uterus Obstetrics and Gynecology medicine.disease Fibronectins female genital diseases and pregnancy complications Extracellular Matrix Tumor Burden Cell biology Gene Expression Regulation Neoplastic 030104 developmental biology Reproductive Medicine Uterine Neoplasms Female Stress Mechanical Glycoprotein Hormone |
| Zdroj: | Seminars in Reproductive Medicine. 35:487-493 |
| ISSN: | 1526-4564 1526-8004 |
| DOI: | 10.1055/s-0037-1607268 |
| Popis: | Fibroids (uterine leiomyomas) are the most common benign tumors of the female reproductive tract. Steroid hormones, growth factors, and cytokines have long been implicated in fibroid growth; however, research suggests that changes in the extracellular matrix and mechanical signaling play a critical role in fibroid growth and differentiation. Studies have shown that growth of fibroids is related to the change in the volume and composition of extracellular matrix with increased deposition of abnormal collagen, glycoproteins, laminins, fibronectins, and an increased osmotic stress. These changes generate mechanical stress which is converted to chemical signals in the cells through mechanotransduction and eventually affects gene expression and protein synthesis. Current studies also suggest that mechanical signaling in fibroid cells is abnormal as evidenced by decreased apoptosis of abnormal cells and deposition of a stiff extracellular matrix promoting fibrosis. Understanding and defining these mechanisms could help design new therapies for the treatment of fibroids. |
| Databáze: | OpenAIRE |
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