AI Article Synopsis
- The study investigates the link between gestational diabetes mellitus (GDM) and preeclampsia (PE), focusing on the role of oxidative stress and protein acetylation in their development.
- Researchers analyzed placental tissues from healthy individuals and patients with GDM and PE, identifying 22 regulated proteins and 192 acetylated proteins that are significant to these conditions.
- The findings highlight the involvement of endoplasmic reticulum stress and ferroptosis pathways, offering potential insights into biomarkers and therapeutic targets for GDM and PE.
Article Abstract
Gestational diabetes mellitus (GDM) and preeclampsia (PE) are associated with maternal and infant health. Although the pathogenesis of PE and GDM remains controversial, oxidative stress is involved in the underlying pathology of GDM and PE. Protein lysine acetylation (Kac) plays an important regulatory role in biological processes. There is little data regarding the association of the maternal acetylome with GDM and PE. This study aimed to assess the potential value of the proteome and acetylome for GDM and PE. In our study, we included placental tissues from healthy individuals (n = 6), GDM patients (n = 6), and PE patients (n = 6) to perform 4D-label free quantification proteomics analysis and PRM analysis. We identified 22 significantly regulated proteins and 192 significantly regulated acetylated proteins between the GDM and PE groups. Furthermore, 192 significantly regulated acetylated proteins were mainly enriched in endoplasmic reticulum stress (ERS) and ferroptosis pathways. Seventeen acetylated sites in these two pathways were verified by PRM analysis. Our comprehensive analysis revealed key features of GDM/PE-significantly regulated acetylated proteins in the placentas from GDM and PE. The results of signaling pathway analysis focused on ERS and ferroptosis. These findings may help explore the underlying pathology, new biomarkers, and therapeutic targets of GDM and PE.
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| http://dx.doi.org/10.1002/pmic.202200124 | DOI Listing |
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