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Biomolecules
Special Issues
Placental-Related Disorders of Pregnancy II
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Placental-Related Disorders of Pregnancy II

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 15 September 2024 | Viewed by 1415

Special Issue Editor

Dr. Zaneta Kimber-Trojnar

E-Mail Website
Guest Editor
Chair and Department of Obstetrics and Perinatology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: gestational diabetes mellitus; fetal growth restriction; preeclampsia biomarkers; preterm delivery; fetal programming; excessive gestational weight gain; metabolic syndrome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a very successful first run, we are pleased to announce the launch of a second edition of a Special Issue entitled “Placental-Related Disorders of Pregnancy”.

The placenta is a unique, multifunctional organ that develops exclusively in pregnancy and results from complex interactions between the tissues of the fetus and the mother. It is responsible for exchanging nutrients, gases and wastes between the maternal and fetal circulations. The placenta is also an important endocrine organ that produces hormones indispensable to supporting pregnancy and regulating feto-maternal physiology. The main function of the placenta, however, is to maintain the environmental homeostasis required for fetal growth.

Placental-related disorders, which affect about a third of human pregnancies, manifest via different symptoms diseases and complications. Examples of these illnesses include preeclampsia, intrauterine growth restriction, placental abruption and placenta accreta, all of which contribute to increased maternal and perinatal morbidity and mortality. Placental dysfunction and programming may also have lifelong health consequences for both mother and offspring. Delayed reproductive plans, the incidence of cesarean sections, and lifestyle changes, including improper diet, appear to have increased the incidence of placental-related disorders and diseases in recent decades.

We invite the scientific community to submit original articles and reviews on placentation and placental-related disorders to provide some novel insight into any aspect of placental biochemistry. We believe that, with your input, this Special Issue will shed more light on the mechanisms involved in the development of placental pathologies and help to find biomolecules for their prediction and early diagnosis.

Dr. Zaneta Kimber-Trojnar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • placenta
  • preeclampsia
  • intrauterine growth restriction
  • placental abruption
  • placenta accrete
  • biomolecules
  • fetal programming
  • maternal programming
  • endothelial dysfunction
  • inflammation
  • oxidative stress

Related Special Issue

Published Papers (1 paper)

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Research

17 pages, 21708 KiB  
Article
High Glucose Promotes and Aggravates the Senescence and Dysfunction of Vascular Endothelial Cells in Women with Hyperglycemia in Pregnancy
by Lin Zheng, Mingqing Li and Huaping Li
Biomolecules 2024, 14(3), 329; https://doi.org/10.3390/biom14030329 - 10 Mar 2024
Viewed by 1083
Abstract
Hyperglycemia in pregnancy (HIP) is linked to fetoplacental endothelial dysfunction, which might be a result of hyperglycemia. Hyperglycemia is associated with cell senescence; however, the role and mechanism of high glucose and cell senescence in HIP endothelial cell failure are largely unknown. Our [...] Read more.
Hyperglycemia in pregnancy (HIP) is linked to fetoplacental endothelial dysfunction, which might be a result of hyperglycemia. Hyperglycemia is associated with cell senescence; however, the role and mechanism of high glucose and cell senescence in HIP endothelial cell failure are largely unknown. Our study discovered that human umbilical vein endothelial cells (HUVECs) obtained from HIP pregnant women exhibit excessive senescence, with significantly elevated expression of senescence markers senescence-associated beta-galactosidase (SA-β-gal), p16, p21, and p53. Subsequently, we found that exposing primary HUVECs and cell lines to high glucose resulted in an increase in the synthesis of these senescence indicators, similar to what had been observed in pregnant women with HIP. A replicate senescence model and stress-induced premature senescence (SIPS) model showed higher amounts of vascular damage indicators, including von Willebrand factor (vWF), chemotactic C-C motif chemokine ligand 2 (CCL2), intercellular adhesion molecule 1 (ICAM-1), along with the anti-apoptotic protein BCL2. However, lower expressions of the pro-apoptotic component BAX, in addition to defective proliferation and tubulogenesis, were seen. Further studies indicated that hyperglycemia can not only induce these alterations in HUVECs but also exacerbate the aforementioned changes in both aging HUVECs. The experiments outlined above have also been validated in pregnant women with HIP. Collectively, these data suggest that exposure to high glucose accelerates cell senescence-mediated vein endothelial cell dysfunction, including excessive inflammation, cell adhesion, impaired angiogenesis, and cell proliferation possibly contributing to pregnancy complications and adverse pregnancy outcomes. Full article
(This article belongs to the Special Issue Placental-Related Disorders of Pregnancy II)
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