Description

Our last goal was the identification of the molecular profile associated with in vivo defective decidualization in severe preeclampsia (sPE). We discover the transcriptomic footprint encoding in vivo decidualization defect that implicates a dysregulated progesterone and estradiol signaling (eLIFE 2021). These findings reinforce the maternal contribution to sPE opening new avenues to understand the origin and causes underlaying this defect. Therefore, the main objectives of this research line are:

  • Dislucidate the molecular mechanisms that govern the origin and causes of the maternal defective decidualization with the aim to develop therapies focused on improving this process and preventing preeclampsia.
  • Decode the molecular atlas of defective decidualization in sPE at cell resolution. We will apply single-cell transcriptomics and the development of a three-dimensional model able to mimic the cellular complexity characteristic of this defect.

Principal Investigator

Main Publications

Some of the main collaborative projects with internationally-renowned centres include:

External Funding and Grants

Some of the main collaborative projects with internationally-renowned centres include:

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Research on Reproductive Medicine, focusing on genomics,
bioinformatics and the factors that affect human reproduction.

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