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Pathophysiological Research into and Treatment of Pregnancy Complications
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Pathophysiological Research into and Treatment of Pregnancy Complications

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: 20 April 2025 | Viewed by 8377

Special Issue Editor

Dr. Te-Fu Chan

E-Mail Website
Guest Editor
1. Graduate Institute of Medicine, College of Medicine & Drug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung 807378, Taiwan
2. Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung 807377, Taiwan
Interests: high-risk pregnancies; perinatal medicine; genetic diagnosis; obstetrics and gynecology; endocrinology of reproduction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Common complications of pregnancy include preterm labor, placental abruption, pre-eclampsia and gestational diabetes. Managing these conditions during pregnancy is crucial. Beyond that, it is important to acknowledge that these conditions may recur in subsequent pregnancies. Furthermore, pregnancy complications can have implications for the long-term health of the mother.

Early diagnosis and prevention are paramount. Molecular-level research contributes to a deeper understanding of the molecular mechanisms of diseases, enabling the development of more precise diagnostic methods and prevention and treatment strategies targeted at specific molecular markers. We welcome all innovative studies offering valuable insights for the benefit of the scientific community.

Dr. Te-Fu Chan
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. 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

  • complications of pregnancy
  • preterm labor
  • placental abruption
  • pre-eclampsia
  • gestational diabetes

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Published Papers (2 papers)

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Research

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14 pages, 2976 KiB  
Article
Maternal Obesity Alters Placental and Umbilical Cord Plasma Oxidative Stress, a Cross-Sectional Study
by Thanyawan Jantape, Kiattisak Kongwattanakul, Silvia M. Arribas, Pilar Rodríguez-Rodríguez, Metee Iampanichakul, Wannapa Settheetham-Ishida and Sophida Phuthong
Int. J. Mol. Sci. 2024, 25(19), 10866; https://doi.org/10.3390/ijms251910866 - 9 Oct 2024
Viewed by 1016
Abstract
Maternal obesity has been shown to impair the oxidative status in the placenta and newborns, potentially leading to adverse pregnancy outcomes and long-term effects on the programming of offspring metabolic status. This study aimed to investigate the impact of maternal obesity on maternal [...] Read more.
Maternal obesity has been shown to impair the oxidative status in the placenta and newborns, potentially leading to adverse pregnancy outcomes and long-term effects on the programming of offspring metabolic status. This study aimed to investigate the impact of maternal obesity on maternal and umbilical cord plasma oxidative status, as well as placental oxidative adaptation. Maternal obesity (n = 20), defined as a pre-pregnancy BMI ≥ 25 kg/m2, and maternal leanness (n = 20), defined as a pre-pregnancy BMI < 23 kg/m2, were the group categories used in this study. Both groups were matched according to gestational age at delivery. Maternal blood, umbilical cord blood, and placental tissue were collected to assess nutritional content (cholesterol, triglyceride, and protein), oxidative stress markers (MDA and protein carbonyl), and antioxidant activity (SOD and catalase). Placental protein expression (SOD2, catalase, UCP2, and Nrf2) was evaluated using Western blot analysis. Catalase activity in maternal plasma significantly increased in the maternal obesity group (p = 0.0200), with a trend toward increased MDA and protein carbonyl levels. In umbilical cord plasma, triglyceride, protein carbonyl, and catalase activity were significantly elevated in the maternal obesity group compared with the lean controls (p = 0.0482, 0.0291, and 0.0347, respectively). Placental protein expression analysis revealed significantly decreased SOD2 (p = 0.0011) and catalase (p < 0.0001), along with Nrf2 downregulation (p < 0.0001). An increase in mitochondrial antioxidant UCP2 expression was observed (p = 0.0117). The neonatal protein carbonyl levels positively correlated with placental protein carbonyl (r = 0.7405, p < 0.0001) and negatively correlated with maternal catalase activity (r = −0.4332, p = 0.0052). This study thus provides evidence that maternal obesity is associated with placental and fetal oxidative stress, alongside a concurrent increase in placental antioxidant UCP2 expression. Full article
(This article belongs to the Special Issue Pathophysiological Research into and Treatment of Pregnancy Complications)
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Review

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24 pages, 1162 KiB  
Review
A Narrative Review on the Pathophysiology of Preeclampsia
by Johnatan Torres-Torres, Salvador Espino-y-Sosa, Raigam Martinez-Portilla, Hector Borboa-Olivares, Guadalupe Estrada-Gutierrez, Sandra Acevedo-Gallegos, Erika Ruiz-Ramirez, Martha Velasco-Espin, Pablo Cerda-Flores, Andrea Ramirez-Gonzalez and Lourdes Rojas-Zepeda
Int. J. Mol. Sci. 2024, 25(14), 7569; https://doi.org/10.3390/ijms25147569 - 10 Jul 2024
Cited by 4 | Viewed by 6812
Abstract
Preeclampsia (PE) is a multifactorial pregnancy disorder characterized by hypertension and proteinuria, posing significant risks to both maternal and fetal health. Despite extensive research, its complex pathophysiology remains incompletely understood. This narrative review aims to elucidate the intricate mechanisms contributing to PE, focusing [...] Read more.
Preeclampsia (PE) is a multifactorial pregnancy disorder characterized by hypertension and proteinuria, posing significant risks to both maternal and fetal health. Despite extensive research, its complex pathophysiology remains incompletely understood. This narrative review aims to elucidate the intricate mechanisms contributing to PE, focusing on abnormal placentation, maternal systemic response, oxidative stress, inflammation, and genetic and epigenetic factors. This review synthesizes findings from recent studies, clinical trials, and meta-analyses, highlighting key molecular and cellular pathways involved in PE. The review integrates data on oxidative stress biomarkers, angiogenic factors, immune interactions, and mitochondrial dysfunction. PE is initiated by poor placentation due to inadequate trophoblast invasion and improper spiral artery remodeling, leading to placental hypoxia. This triggers the release of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), causing widespread endothelial dysfunction and systemic inflammation. Oxidative stress, mitochondrial abnormalities, and immune dysregulation further exacerbate the condition. Genetic and epigenetic modifications, including polymorphisms in the Fms-like tyrosine kinase 1 (FLT1) gene and altered microRNA (miRNA) expression, play critical roles. Emerging therapeutic strategies targeting oxidative stress, inflammation, angiogenesis, and specific molecular pathways like the heme oxygenase-1/carbon monoxide (HO-1/CO) and cystathionine gamma-lyase/hydrogen sulfide (CSE/H2S) pathways show promise in mitigating preeclampsia’s effects. PE is a complex disorder with multifactorial origins involving abnormal placentation, endothelial dysfunction, systemic inflammation, and oxidative stress. Despite advances in understanding its pathophysiology, effective prevention and treatment strategies remain limited. Continued research is essential to develop targeted therapies that can improve outcomes for both mothers and their babies. Full article
(This article belongs to the Special Issue Pathophysiological Research into and Treatment of Pregnancy Complications)
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