ArticleBMC biology2024
Monoamine oxidases activity maintains endometrial monoamine homeostasis and participates in embryo implantation and development.
Article in BMC biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The placental tryptophan pathway across gestation: implications for pregnancy outcomes.Human reproduction update · 2026Review
- Compensatory Serotonin Synthesis and Histone H3 Serotonylation in Preimplantation Embryos Exposed to Maternal Fluoxetine or Monoamine Oxidase Blockade.Journal of developmental biology · 2026Article
- Male Stress Is Associated with Ovarian and Endometrial Responses in ICSI Cycles: Is Seminal Plasma the Linchpin?International journal of molecular sciences · 2026Article
- Atlas-scale metabolic activities inferred from single-cell and spatial transcriptomics.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundMonoamine oxidases (MAOs) is an enzyme that catalyzes the deamination of monoamines. The current research on this enzyme is focused on its role in neuropsychiatric, neurodevelopmental, and neurodegenerative diseases. Indeed, MAOs with two isoforms, namely, A and B, are located on the outer mitochondrial membrane and are widely distributed in the central nervous system and peripheral tissues. Several reports have described periodic changes in the levels of this enzyme in the human endometrial tissue.
resultsThe novel role of MAOs in endometrial receptivity establishment and embryonic development by maintaining monoamine homeostasis was investigated in this study. MAOs activity was observed to be enhanced during the first trimester in both humans and mice under normal conditions. However, under pathological conditions, MAOs activity was reduced and was linked to early pregnancy failure. During the secretory phase, the endometrial stromal cells differentiated into decidual cells with a stronger metabolism of monoamines by MAOs. Excessive monoamine levels cause monoamine imbalance in decidual cells, which results in the activation of the AKT signal, decreased FOXO1 expression, and decidual dysfunction.
conclusionsThe findings suggest that endometrial receptivity depends on the maintenance of monoamine homeostasis via MAOs activity and that this enzyme participates in embryo implantation and development.
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