Unveiling the role of microRNAs in metabolic dysregulation of Gestational Diabetes Mellitus
Reproductive Biology, ISSN: 1642-431X, Vol: 24, Issue: 3, Page: 100924
2024
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
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Review Description
Gestational Diabetes Mellitus (GDM) presents a significant health concern globally, necessitating a comprehensive understanding of its metabolic intricacies for effective management. MicroRNAs (miRNAs) have emerged as pivotal regulators in GDM pathogenesis, influencing glucose metabolism, insulin signaling, and lipid homeostasis during pregnancy. Dysregulated miRNA expression, both upregulated and downregulated, contributes to GDM-associated metabolic abnormalities. Ethnic and temporal variations in miRNA expression underscore the multifaceted nature of GDM susceptibility. This review examines the dysregulation of miRNAs in GDM and their regulatory functions in metabolic disorders. We discuss the involvement of specific miRNAs in modulating key pathways implicated in GDM pathogenesis, such as glucose metabolism, insulin signaling, and lipid homeostasis. Furthermore, we explore the potential diagnostic and therapeutic implications of miRNAs in GDM management, highlighting the promise of miRNA-based interventions for mitigating the adverse consequences of GDM on maternal and offspring health.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1642431X24000706; http://dx.doi.org/10.1016/j.repbio.2024.100924; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85198534420&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/39013209; https://linkinghub.elsevier.com/retrieve/pii/S1642431X24000706
Elsevier BV
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