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Physiology and Pathophysiology of Placenta: 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 1025

Special Issue Editor


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Guest Editor
Department of Experimental and Clinical Medicine, Polytechnic University of Marche, Via Tronto, 10/a, 60126 Ancona, Italy
Interests: pregnancy complications; preeclampsia; preterm birth; ovarian cancer; early marker of pregnancy complications; oxidative stress; chemoresistance
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Special Issue Information

Dear Colleagues,

This is a continued series of the hot topic of "Physiology and Pathophysiology of Placenta". We already have done successful special issues that received interesting contributions and discussions.

The development and differentiation of placental villous tree are two key process tightly regulated during pregnancy. In fact, several growth factors, their receptors and other types of molecules can regulate placental cell proliferation, differentiation, migration and invasion. Thus, an impairment of normal placental development can lead to a series of pregnancy pathologies, i.e., preeclampsia (PE), fetal growth restriction (FGR), gestational trophoblastic diseases (GTD) and gestational diabetes mellitus (GDM). Furthermore, external factors, such as microbial agents, chemicals and natural compounds can affect placental development and function impairing pregnancy outcome.

These pregnancy complications result in increased maternal and fetal mortality and morbidity leading to life-long health implications in both mother and child.

The aim of this Special Issue is to provide an overview of the placental development and pathophysiology in order to better understand the molecular mechanisms involved in pregnancy. We are inviting submissions of original research articles, reviews and mini-reviews on topics relevant to any aspect of placental physiology, pathophysiology, biochemistry and molecular biology.

Dr. Giovanni Tossetta
Guest Editor

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • trophoblast
  • proliferation
  • differentiation
  • invasion
  • placenta
  • preeclampsia
  • fetal growth restriction
  • gestational diabetes mellitus
  • infection
  • pregnancy complications

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Published Papers (2 papers)

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Research

10 pages, 567 KiB  
Article
Disparity Between Functional and Structural Recovery of Placental Mitochondria After Exposure to Hypoxia
by Jonathan R. Sierla, Laia Pagerols Raluy, Magdalena Trochimiuk, Julian Trah, Mariam Petrosyan, Lis N. Velasquez, Udo Schumacher, Dominique Singer and Julia Heiter
Int. J. Mol. Sci. 2025, 26(7), 2956; https://doi.org/10.3390/ijms26072956 - 25 Mar 2025
Viewed by 282
Abstract
Intrauterine growth restriction (IUGR) affects 5–10% of pregnancies with placental hypoxia, playing a key role as a common pathophysiological pathway of different etiologies. Despite the high metabolic rate of the placenta and its “gatekeeper” role in protecting the fetus from hypoxia, the response [...] Read more.
Intrauterine growth restriction (IUGR) affects 5–10% of pregnancies with placental hypoxia, playing a key role as a common pathophysiological pathway of different etiologies. Despite the high metabolic rate of the placenta and its “gatekeeper” role in protecting the fetus from hypoxia, the response of placental mitochondria to hypoxic stress is not well understood. This study tested the hypothesis that transient exposure to hypoxia leads to a loss of placental mitochondria and affects their function. Human villous trophoblastic (JEG-3) cells were cultured under normoxic and hypoxic conditions for 24 h. Mitochondrial content was determined by flow cytometry before and after hypoxic exposure and after 24 h of normoxic recovery. Parameters of oxidative phosphorylation were assessed using a respirometric analyzer before hypoxic exposure and after normoxic recovery. Mitochondrial content decreased significantly from 88.5% to 26.7% during hypoxic incubation. Although it had increased to 84.2% after 24 h of normoxic recovery, oxidative phosphorylation parameters were still significantly suppressed to 1/2 to 1/3 of the pre-incubation levels. The results underscore the ability of placental cells to adapt mitochondrial content to O2 supply. Despite rapid recovery under normoxia, respiratory function remains suppressed, which may result in persistent impairment of adenosine triphosphate (ATP)-dependent synthetic and transport functions. Full article
(This article belongs to the Special Issue Physiology and Pathophysiology of Placenta: 3rd Edition)
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17 pages, 10161 KiB  
Article
Placental Molecular Expression of Different Pathogenic Vaginal Infections
by Daniela Roxana Matasariu, Constantin Condac, Victoria Bîrluțiu, Ludmila Lozneanu, Iuliana Elena Bujor, Vasile Lucian Boiculese, Mihai Sava and Alexandra Ursache
Int. J. Mol. Sci. 2025, 26(7), 2863; https://doi.org/10.3390/ijms26072863 - 21 Mar 2025
Viewed by 343
Abstract
This study evaluated the differential expression of four placental markers—vitamin D receptor (VDR), Cluster of Differentiation 44 (CD44), osteopontin (OPN), and cyclooxygenase-2 (COX-2)—in response to pathogens, which may contribute to our understanding of pathogen-specific impacts on pregnancy outcomes. We immunohistochemically (IHC) analyzed placental [...] Read more.
This study evaluated the differential expression of four placental markers—vitamin D receptor (VDR), Cluster of Differentiation 44 (CD44), osteopontin (OPN), and cyclooxygenase-2 (COX-2)—in response to pathogens, which may contribute to our understanding of pathogen-specific impacts on pregnancy outcomes. We immunohistochemically (IHC) analyzed placental tissues obtained from 70 healthy-term pregnant women in the control group and compared them to tissues obtained from 78 women with pregnancy above 24 weeks of gestation, single-pathogen vaginal infection, and premature rupture of membranes/preterm premature rupture of membranes (PROM/PPROM). We detected high expression of these four molecules in cases of Group B Streptococcus (GBS) and Ureaplasma urealyticum vaginal infections, and moderate expression in cases of Enterobacteriaceae infections, except for Klebsiella; the cases with Klebsiella and Candida species (spp.) vaginitis exhibited a lower expression compared to the healthy control group. VDR, CD44, and OPN had increased placental expression in GBS and Ureaplasma urealyticum vaginal infections; the opportunistic pathogenicity of both Escherichia coli and Candida spp. explains their low IHC positivity, and the tremendous ability of Gram-negative bacteria to elude the host immunity is revealed by the negative IHC staining in cases of Klebsiella vaginitis. These findings suggest that pathogen-specific alterations in the expression of these markers may contribute to the differential risk stratification of pregnancy complications and may mitigate the risks of adverse maternal and fetal outcomes. Interventions aiming to modulate these pathways might improve pregnancy outcomes. Full article
(This article belongs to the Special Issue Physiology and Pathophysiology of Placenta: 3rd Edition)
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