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miR-181a-5p: a key regulator of placental function in health and disease
Leisa Lopes-Aguiar1, Rafaella Scandiuzzi1, Gabriela Michelazzo1
1Department of Biochemistry and Tissue Biology, Biology Institute, University of Campinas, Campinas, Brazil.
MicroRNAs (miRNAs) are essential post-transcriptional regulators implicated in diverse physiological and pathological processes. Recently, miR-181a-5p emerged as a critical modulator of placental function. This review synthesizes literature on miR-181a-5p at the maternal-foetal interface in normal pregnancies and complications, such as preeclampsia, gestational hypertension, gestational diabetes, and Rh-negative haemolytic disease of the foetus and newborn (Rh-HDFN). From a PubMed search, 12 articles were qualitatively synthesized. Evidence shows that early miR-181a-5p suppression is crucial for normal trophoblast proliferation via the renin-angiotensin system. Conversely, its aberrant expression characterizes gestational pathologies. In preeclampsia, miR-181a-5p upregulation suppresses trophoblast viability, migration, and invasion, increasing apoptosis. In gestational hypertension, its downregulation perturbs glycolytic metabolism. Furthermore, elevated miR-181a-5p disrupts endothelial and placental barriers in gestational diabetes and Rh-HDFN, respectively. Ultimately, miR-181a- as a pleiotropic regulator in the placenta. Decoding its molecular networks underscores its clinical potential as a biomarker and therapeutic target.
MicroRNAs (miRNAs) are essential post-transcriptional regulators implicated in diverse physiological and pathological processes. Recently, miR-181a-5p emerged as a critical modulator of placental function. This review synthesizes literature on miR-181a-5p at the maternal-foetal interface in normal pregnancies and complications, such as preeclampsia, gestational hypertension, gestational diabetes, and Rh-negative haemolytic disease of the foetus and newborn (Rh-HDFN). From a PubMed search, 12 articles were qualitatively synthesized. Evidence shows that early miR-181a-5p suppression is crucial for normal trophoblast proliferation via the renin-angiotensin system. Conversely, its aberrant expression characterizes gestational pathologies. In preeclampsia, miR-181a-5p upregulation suppresses trophoblast viability, migration, and invasion, increasing apoptosis. In gestational hypertension, its downregulation perturbs glycolytic metabolism. Furthermore, elevated miR-181a-5p disrupts endothelial and placental barriers in gestational diabetes and Rh-HDFN, respectively. Ultimately, miR-181a- as a pleiotropic regulator in the placenta. Decoding its molecular networks underscores its clinical potential as a biomarker and therapeutic target.
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