{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nAlthough none of the provided abstracts mention MIR8052 explicitly, the collective body of work on monoamine oxidase–related pathways suggests a role for regulatory molecules—potentially including microRNAs such as MIR8052—in fine‐tuning the expression and activity of MAO‐A. MAO‐A is a mitochondrial enzyme responsible for the oxidative degradation of key monoamine neurotransmitters (serotonin, norepinephrine, dopamine) and is critically involved in circadian regulation, mood modulation, and behavioral responses. Several studies report that factors including circadian clock components and transcriptional regulators (for example, SIRT1 and R1) modulate MAO‐A promoter activity and hence influence neurotransmitter levels and behavioral phenotypes such as reactive aggression and mood‐related disturbances."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nOther investigations have focused on the role of MAO‐A in non‐neuronal settings—for instance, its contribution to reactive oxygen species generation, mitochondrial dysfunction, and apoptosis in cardiomyocytes. These studies demonstrate that aberrant MAO‐A activity is linked to altered sphingolipid metabolism and impaired autophagic processes, ultimately contributing to cardiac injury and age‐related cellular senescence. Regulatory inputs that control MAO‐A expression may therefore be crucial not only in modulating neurotransmission but also in maintaining cellular homeostasis under metabolic or stress conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the realm of neurodevelopment and behavioral adaptation, excess or deficient MAO‐A activity has been associated with disrupted formation of neural circuits (as seen in altered thalamocortical projections and sensory cortical organization) and with behavioral phenotypes relevant to autism spectrum and impulse control disorders. Although the reviewed abstracts predominantly address protein and transcription factor regulators of MAO‐A, by analogy a microRNA such as MIR8052 could be hypothesized to partake in the post‐transcriptional regulation of MAO‐A expression—thereby indirectly influencing neuronal proliferation, circuit refinement, and subsequent behavioral outcomes including social interaction, aggression, and stress responsiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTaken together, while the function of MIR8052 is not directly delineated in these studies, its potential involvement in the post‐transcriptional regulation of MAO‐A (and perhaps related pathways) emerges as an attractive hypothesis. Regulation of MAO‐A by microRNAs could influence multiple physiological systems—from circadian and metabolic control to neurodevelopment and stress adaptation—and may thus contribute to disease states such as depression, anxiety, autism spectrum disorders, and cardiac dysfunction."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Gabriele Hampp, Jürgen A Ripperger, Thijs Houben, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Regulation of monoamine oxidase A by circadian-clock components implies clock influence on mood."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Curr Biol (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cub.2008.04.012"}], "href": "https://doi.org/10.1016/j.cub.2008.04.012"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18439826"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18439826"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Sergiy Libert, Kelli Pointer, Eric L Bell, et al. "}, {"type": "b", "children": [{"type": "t", "text": "SIRT1 activates MAO-A in the brain to mediate anxiety and exploratory drive."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cell.2011.10.054"}], "href": "https://doi.org/10.1016/j.cell.2011.10.054"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22169038"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22169038"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Nina Kaludercic, Eiki Takimoto, Takahiro Nagayama, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase A-mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Circ Res (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/CIRCRESAHA.109.198366"}], "href": "https://doi.org/10.1161/CIRCRESAHA.109.198366"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19910579"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19910579"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Dimitri Pchejetski, Oxana Kunduzova, Audrey Dayon, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Circ Res (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/01.RES.0000253900.66640.34"}], "href": "https://doi.org/10.1161/01.RES.0000253900.66640.34"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17158340"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17158340"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Alexandra Rebsam, Isabelle Seif, Patricia Gaspar "}, {"type": "b", "children": [{"type": "t", "text": "Refinement of thalamocortical arbors and emergence of barrel domains in the primary somatosensory cortex: a study of normal and monoamine oxidase a knock-out mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurosci (2002)"}]}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12351728"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12351728"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Xiao-Ming Ou, Kevin Chen, Jean C Shih "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase A and repressor R1 are involved in apoptotic signaling pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Proc Natl Acad Sci U S A (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1073/pnas.0601515103"}], "href": "https://doi.org/10.1073/pnas.0601515103"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16829576"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16829576"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Nina Kaludercic, Andrea Carpi, Takahiro Nagayama, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Antioxid Redox Signal (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1089/ars.2012.4616"}], "href": "https://doi.org/10.1089/ars.2012.4616"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23581564"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23581564"}]}, {"type": "r", "ref": 8, "children": [{"type": "t", "text": "Kevin Chen, Daniel P Holschneider, Weihua Wu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M405550200"}], "href": "https://doi.org/10.1074/jbc.M405550200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15272015"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15272015"}]}, {"type": "r", "ref": 9, "children": [{"type": "t", "text": "Marco Bortolato, Sean C Godar, Loai Alzghoul, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase A and A/B knockout mice display autistic-like features."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Neuropsychopharmacol (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1017/S1461145712000715"}], "href": "https://doi.org/10.1017/S1461145712000715"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22850464"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22850464"}]}, {"type": "r", "ref": 10, "children": [{"type": "t", "text": "Anna L Scott, Marco Bortolato, Kevin Chen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Novel monoamine oxidase A knock out mice with human-like spontaneous mutation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neuroreport (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1097/WNR.0b013e3282fd6e88"}], "href": "https://doi.org/10.1097/WNR.0b013e3282fd6e88"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18418249"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18418249"}]}, {"type": "r", "ref": 11, "children": [{"type": "t", "text": "Yohan Santin, Pierre Sicard, François Vigneron, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Oxidative Stress by Monoamine Oxidase-A Impairs Transcription Factor EB Activation and Autophagosome Clearance, Leading to Cardiomyocyte Necrosis and Heart Failure."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Antioxid Redox Signal (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1089/ars.2015.6522"}], "href": "https://doi.org/10.1089/ars.2015.6522"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26959532"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26959532"}]}, {"type": "r", "ref": 12, "children": [{"type": "t", "text": "Adrian Sturza, Matthias S Leisegang, Andrea Babelova, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidases are mediators of endothelial dysfunction in the mouse aorta."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hypertension (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/HYPERTENSIONAHA.113.01314"}], "href": "https://doi.org/10.1161/HYPERTENSIONAHA.113.01314"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23670301"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23670301"}]}, {"type": "r", "ref": 13, "children": [{"type": "t", "text": "Nicola Manzella, Yohan Santin, Damien Maggiorani, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase-A is a novel driver of stress-induced premature senescence through inhibition of parkin-mediated mitophagy."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Aging Cell (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/acel.12811"}], "href": "https://doi.org/10.1111/acel.12811"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30003648"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30003648"}]}, {"type": "r", "ref": 14, "children": [{"type": "t", "text": "Marco Bortolato, Kevin Chen, Sean C Godar, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Social deficits and perseverative behaviors, but not overt aggression, in MAO-A hypomorphic mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neuropsychopharmacology (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/npp.2011.157"}], "href": "https://doi.org/10.1038/npp.2011.157"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21832987"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21832987"}]}, {"type": "r", "ref": 15, "children": [{"type": "t", "text": "Christina S Barr, Melanie L Schwandt, Timothy K Newman, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The use of adolescent nonhuman primates to model human alcohol intake: neurobiological, genetic, and psychological variables."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Ann N Y Acad Sci (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1196/annals.1308.027"}], "href": "https://doi.org/10.1196/annals.1308.027"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15251892"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15251892"}]}, {"type": "r", "ref": 16, "children": [{"type": "t", "text": "Soni Deshwal, Marleen Forkink, Chou-Hui Hu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Monoamine oxidase-dependent endoplasmic reticulum-mitochondria dysfunction and mast cell degranulation lead to adverse cardiac remodeling in diabetes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Differ (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41418-018-0071-1"}], "href": "https://doi.org/10.1038/s41418-018-0071-1"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29459772"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29459772"}]}, {"type": "r", "ref": 17, "children": [{"type": "t", "text": "Chun-Peng Liao, Tzu-Ping Lin, Pei-Chuan Li, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Loss of MAOA in epithelia inhibits adenocarcinoma development, cell proliferation and cancer stem cells in prostate."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncogene (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41388-018-0325-x"}], "href": "https://doi.org/10.1038/s41388-018-0325-x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29844571"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29844571"}]}, {"type": "r", "ref": 18, "children": [{"type": "t", "text": "Olivier Lairez, Denis Calise, Pascale Bianchi, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Genetic deletion of MAO-A promotes serotonin-dependent ventricular hypertrophy by pressure overload."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Mol Cell Cardiol (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.yjmcc.2008.12.017"}], "href": "https://doi.org/10.1016/j.yjmcc.2008.12.017"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19162038"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19162038"}]}]}]}