مقالات پذیرفته شده در هشتمین کنگره بین المللی زیست پزشکی
The Role of miR-133b, miR-125b, and miR-320 in the Pathogenesis of Endometriosis: A Comprehensive Review
The Role of miR-133b, miR-125b, and miR-320 in the Pathogenesis of Endometriosis: A Comprehensive Review
Hadis Farokhdel,1Mahtab Maleki,2Shamim Siavoshpour,3Sara Sharifi Ghombavani,4,*Haniyeh Motie Arani,5
1. Department of biology, Central Tehran Branch, Islamic Azad University, Tehran, Iran 2. Department of Biology, Science and Research Branch , Islamic Azad University , Tehran , Iran 3. Department of biology, Yadegar-e-Imam khomeini, shahre Rey Branch, Islamic Azad University, Tehran, Iran 4. Department of Biology, Science and Research Branch , Islamic Azad University , Tehran , Iran 5. Department of Biochemistry and Biophysics, Faculty of advanced Science and technology, Islamic Azad University, Tehran Medical Sciences. Tehran, Iran
Introduction: Endometriosis is a chronic, estrogen-dependent, inflammatory disease characterized by the presence of endometrial-like tissue outside the uterine cavity, leading to pain, infertility, and reduced quality of life. MicroRNAs (miRNAs) are small, non-coding RNA molecules that play crucial roles in regulating gene expression and have been implicated in the pathogenesis of various diseases, including endometriosis. This comprehensive review focuses on the role of miR-133b, miR-125b, and miR-320 in the pathogenesis of endometriosis, highlighting their potential as diagnostic and therapeutic targets.
Methods: A systematic literature search was conducted using PubMed, Scopus, and Web of Science databases to identify studies published between 2010 and 2023 that investigated the expression and functional roles of miR-133b, miR-125b, and miR-320 in endometriosis. The search terms included "endometriosis," "miR-133b," "miR-125b," "miR-320," "microRNA," and "pathogenesis." The retrieved articles were screened based on their relevance to the role of these miRNAs in endometriosis.
Results: The review identified several studies that reported altered expression levels of miR-133b, miR-125b, and miR-320 in endometriotic tissues and fluids compared to normal endometrium. miR-133b was found to be downregulated in endometriotic lesions, affecting the expression of target genes involved in cell proliferation, migration, and invasion. miR-125b was shown to be upregulated in endometriotic tissues, regulating the expression of genes related to inflammation and angiogenesis. miR-320, on the other hand, was found to be downregulated in endometriosis, targeting genes involved in cell cycle progression and apoptosis.
Conclusion: This review provides compelling evidence that miR-133b, miR-125b, and miR-320 play significant roles in the pathogenesis of endometriosis by regulating key biological processes such as cell proliferation, migration, invasion, inflammation, and angiogenesis. These miRNAs may serve as potential biomarkers for the diagnosis and prognosis of endometriosis and could be targeted for therapeutic intervention. Further research is warranted to elucidate the mechanisms by which these miRNAs contribute to the development and progression of endometriosis.