Τίτλος:
Reporting on the Role of miRNAs and Affected Pathways on the Molecular Backbone of Ovarian Insufficiency: A Systematic Review and Critical Analysis Mapping of Future Research
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Ovarian insufficiency is identified as a perplexing entity in the long list of pathologies impairing fertility dynamics. The three distinct classifications of ovarian insufficiency are poor ovarian response, premature ovarian insufficiency/failure, and advanced maternal age, sharing the common denominator of deteriorated ovarian reserve. Despite efforts to define clear lines among the three, the vast heterogeneity and overlap of clinical characteristics renders their diagnosis and management challenging. Lack of a consensus has prompted an empirically based management coupled by uncertainty from the clinicians’ perspective. Profiling of patients in the era of precision medicine seems to be the way forward, while the necessity for a novel approach is underlined. Implicating miRNAs in the quest for patient profiling is promising in light of their fundamental role in cellular and gene expression regulation. To this end, the current study sets out to explore and compare the three pathophysiologies—from a molecular point of view—in order to enable profiling of patients in the context of in vitro fertilization treatment and enrich the data required to practice individualized medicine. Following a systematic investigation of literature, data referring to miRNAs were collected for each patient category based on five included studies. miRNA–target pairs were retrieved from the DIANA-TarBase repository and microT-CDS. Gene and miRNA annotations were derived from Ensembl and miRbase. A subsequent gene-set enrichment analysis of miRNA targets was performed for each category separately. A literature review on the most crucial of the detected pathways was performed to reveal their relevance to fertility deterioration. Results supported that all three pathophysiologies share a common ground regarding the affected pathways, naturally attributed to the common denominator of ovarian insufficiency. As evidenced, miRNAs could be employed to explore the fine lines and diverse nature of pathophysiology since they constitute invaluable biomarkers. Interestingly, it is the differentiation through miRNAs and not through the molecular affected pathways that corresponds to the three distinctive categories. Alarming discrepancies among publications were revealed, pertaining to employment of empirical and arbitrary criteria in categorizing the patients. Following bioinformatic analysis, the final step of the current study consisted of a critical analysis of the molecular data sourced, providing a clear and unique insight into the physiological mechanisms involved. It is our intention to contribute to mapping future research dedicated to ovarian insufficiency and to help researchers navigate the overwhelming information published in molecular studies. © Copyright © 2021 Rapani, Nikiforaki, Karagkouni, Sfakianoudis, Tsioulou, Grigoriadis, Maziotis, Pantou, Voutsina, Pantou, Koutsilieris, Hatzigeorgiou, Pantos and Simopoulou.
Συγγραφείς:
Rapani, A.
Nikiforaki, D.
Karagkouni, D.
Sfakianoudis, K.
Tsioulou, P.
Grigoriadis, S.
Maziotis, E.
Pantou, A.
Voutsina, A.
Pantou, A.
Koutsilieris, M.
Hatzigeorgiou, A.
Pantos, K.
Simopoulou, M.
Περιοδικό:
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Εκδότης:
Frontiers Media S.A
Λέξεις-κλειδιά:
complementary DNA; cyclic AMP; cyclin dependent kinase 1; double stranded DNA; epidermal growth factor; epidermal growth factor receptor 2; estradiol; glycan; glycoprotein; gonadorelin; gonadotropin; growth hormone; hydroxymethylglutaryl coenzyme A reductase; Janus kinase; mammalian target of rapamycin; mammalian target of rapamycin complex 2; microRN 885 5p; microRNA; microRNA 106b5p; microRNA 1180 3p; microRNA 1197; microRNA 122 5p; microRNA 1226 3p; microRNA 1247 5p; microRNA 127 5p; microRNA 129 5p; microRNA 1306 5p; microRNA 133a 3p; microRNA 133b; microRNA 135b 5p; microRNA 139 3p; microRNA 1468 5p; microRNA 1469; microRNA 146a; microRNA 146a 5p; microRNA 15a 5p; microRNA 181a 2 3p; microRNA 181a 3p; microRNA 184; microRNA 193a 5p; microRNA 194 5p; microRNA 199a 3p; microRNA 199a 5p; microRNA 199b 3p; microRNA 20b 5p; microRNA 214 3p; microRNA 214 5p; microRNA 23a 3p; microRNA 23b 5p; microRNA 26b 5p; microRNA 27 5p; microRNA 27a 3p; microRNA 296 5p; microRNA 3120 3p; microRNA 3120 5p; microRNA 3141; microRNA 32 3p; microRNA 326; microRNA 328 3p; microRNA 337 5p; microRNA 34 3p; microRNA 342 3p; microRNA 343 3p; microRNA 3591 3p; microRNA 3614 5p; microRNA 363; microRNA 3664 3p; microRNA 374b 5p; microRNA 374c 3p; microRNA 376a 5p; microRNA 376c 5p; microRNA 378a 3p; microRNA 378d; microRNA 380 5p; microRNA 3960; microRNA 4279; microRNA 4286; microRNA 431 3p; microRNA 4422; microRNA 4433a 3p; microRNA 4433b 3p; microRNA 4448; microRNA 450a 2 3p; microRNA 450b 3p; microRNA 452 5p; microRNA 4700 5p; microRNA 4751; microRNA 483 3p; microRNA 483 5p; microRNA 493 5p; microRNA 497 3p; microRNA 500a 3p; microRNA 501 3p; microRNA 506 3p; microRNA 508 3p; microRNA 508 5p; microRNA 509 3p; microRNA 511 5p; microRNA 513a 5p; microRNA 513b 5p; microRNA 513c 5p; microRNA 532 3p; microRNA 542 3p; microRNA 586; microRNA 6087; microRNA 636; microRNA 6510 3p; microRNA 654 5p; microRNA 655 3p; microRNA 6722 3p; microRNA 6795 5p; microRNA 8079; microRNA 885 5p; mitochondrial DNA; mitogen activated protein kinase; Muellerian inhibiting factor; neurotrophin; oxytocin; parathyroid hormone; phosphatidylinositol 3 kinase; protein BAD; protein bcl 2; protein kinase B; protein p53; protein tyrosine kinase; proteoheparan sulfate; small untranslated RNA; STAT protein; transcription factor FOXO; transforming growth factor beta; tumor necrosis factor receptor associated factor 6; unclassified drug; vasculotropin receptor; Wnt protein, actin filament; adult; AMPK signaling; apoptosis; Article; bioinformatics; cell aging; cell function; cell interaction; controlled study; female; female fertility; gap junction; gene expression; glucose metabolism; hippo signaling; human; in vitro fertilization; infertility therapy; JAK-STAT signaling; maternal age; meiosis; microarray analysis; mitophagy; molecular biology; mTOR signaling; oocyte; oocyte retrieval; ovary follicle development; ovary insufficiency; pathophysiology; Pi3K/Akt signaling; poor ovarian response; pregnancy complication; premature ovarian failure; protein fingerprinting; RNA extraction; RNA sequencing; signal transduction; systematic review; Wnt signaling
DOI:
10.3389/fcell.2020.590106
