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Molecular Insights into the Developmental Origins of Health and Disease, 2nd 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: 30 November 2025 | Viewed by 977

Special Issue Editor

Special Issue Information

Dear Colleagues,

An increasing body of epidemiological, clinical, and experimental evidence supports the notion that the risk of developing chronic, noncommunicable diseases in adulthood is significantly influenced not only by molecular and genetic factors but also by environmental exposures and lifestyle experiences during early life.

Fetal development and infancy are critical windows characterized by rapid organ growth and functional maturation. It is now well recognized that several pathophysiological conditions—including diabetes and cardiovascular disease—that occur in adolescence and adulthood may have their origins during prenatal or postnatal development. While maternal nutrition remains the most widely examined factor affecting fetal development, recent research has also highlighted the important role of paternal stressors in shaping molecular pathways that influence offspring health.

This Special Issue brings together global experts in developmental and molecular programming to present current perspectives and recent advances in understanding the long-term consequences of altered gene expression and molecular modifications of organ systems during critical developmental stages. Of particular interests are studies exploring how nutritional exposures during fetal development can result in transgenerational epigenetic changes, thereby increasing disease susceptibility later in life.

We also welcome contributions addressing the potential for improved maternal nutrition—before and during pregnancy—as a proactive and powerful strategy for the primary prevention of chronic disease in later life. By emphasizing the molecular underpinnings of normal fetal growth and development, this Special Issue aims to illuminate promising directions for early-life interventions with long-term health benefits.

We look forward to your valuable contributions to this important and evolving field.

Dr. Paramjit S. Tappia
Guest Editor

Manuscript Submission Information

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Keywords

  • Developmental Origins of Health and Disease (DOHaD)
  • fetal development
  • maternal nutrition
  • molecular programming
  • epigenetic modifications
  • environmental exposures
  • genetic factors

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Published Papers (1 paper)

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Research

15 pages, 1920 KiB  
Article
The Absence of Bovine Serum Albumin (BSA) in Preimplantation Culture Media Impairs Embryonic Development and Induces Metabolic Alterations in Mouse Offspring
by Jannatul Ferdous Jharna, Md Wasim Bari, Norermi Firzana Alfian and Satoshi Kishigami
Int. J. Mol. Sci. 2025, 26(14), 6989; https://doi.org/10.3390/ijms26146989 - 21 Jul 2025
Viewed by 840
Abstract
Bovine serum albumin (BSA), the most commonly used protein in preimplantation embryo culture media, performs a variety of physiological functions. However, its involvement in long-term effects remains largely unclear. To investigate its physiological importance in culture media, we examined the developmental and metabolic [...] Read more.
Bovine serum albumin (BSA), the most commonly used protein in preimplantation embryo culture media, performs a variety of physiological functions. However, its involvement in long-term effects remains largely unclear. To investigate its physiological importance in culture media, we examined the developmental and metabolic consequences of BSA deprivation during preimplantation stages in mice. Embryos cultured in BSA-free media during specific time windows exhibited impaired blastocyst formation, with continuous deprivation from the two-pronuclei (2PN) stage significantly reducing trophectoderm (TE) and inner cell mass (ICM) cell numbers (p < 0.05), indicating compromised viability. Short-term BSA deprivation similarly disrupted lineage allocation, underscoring the sensitivity of early embryos to nutrient availability during cell fate determination. Although birth rates remained unaffected, suggesting compensatory mechanisms, longitudinal analysis revealed sex-specific metabolic dysfunction. Male offspring developed progressive glucose intolerance by 16 weeks, exhibiting elevated fasting glucose levels (p < 0.05) and impaired glucose clearance, whereas females showed no significant alterations in glucose metabolism. This study demonstrates that protein restriction during the preimplantation period not only disrupts early embryonic development but also programs long-term metabolic dysfunction, underscoring the importance of optimizing culture conditions in assisted reproductive technologies to minimize future health risks. Full article
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