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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 April 2026 | Viewed by 2591

Special Issue Editors


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Guest Editor
1. Asper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada
2. Department of Pharmacology and Therapeutics, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0T6, Canada
Interests: oncology; research; pharmacology; ethics; cancer; cardiology; diabetes; innovation; regulatory
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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
Dr. Bram Ramjiawan
Guest Editors

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

  • 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 (2 papers)

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Research

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15 pages, 1920 KB  
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
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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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Review

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19 pages, 961 KB  
Review
Exercise-Induced Molecular Adaptations in Chronic Non-Communicable Diseases—Narrative Review
by Héctor Fuentes-Barría, Raúl Aguilera-Eguía, Miguel Alarcón-Rivera, Olga López-Soto, Juan Alberto Aristizabal-Hoyos, Ángel Roco-Videla, Marcela Caviedes-Olmos and Diana Rojas-Gómez
Int. J. Mol. Sci. 2025, 26(24), 12096; https://doi.org/10.3390/ijms262412096 - 16 Dec 2025
Abstract
Physical exercise is a potent non-pharmacological strategy for the prevention and management of chronic non-communicable diseases (NCDs), including type 2 diabetes, cardiovascular diseases, obesity, and certain cancers. Growing evidence demonstrates that the benefits of exercise extend beyond its physiological effects and are largely [...] Read more.
Physical exercise is a potent non-pharmacological strategy for the prevention and management of chronic non-communicable diseases (NCDs), including type 2 diabetes, cardiovascular diseases, obesity, and certain cancers. Growing evidence demonstrates that the benefits of exercise extend beyond its physiological effects and are largely mediated by coordinated molecular and cellular adaptations. This review synthesizes current knowledge on the key mechanisms through which exercise modulates metabolic health, emphasizing intracellular signaling pathways, epigenetic regulation, and myokine-driven inter-organ communication. Exercise induces acute and chronic activation of pathways such as AMPK, PGC-1α, mTOR, MAPKs, and NF-κB, leading to enhanced mitochondrial biogenesis, improved oxidative capacity, refined energy sensing, and reduced inflammation. Additionally, repeated muscle contraction stimulates the release of myokines—including IL-6, irisin, BDNF, FGF21, apelin, and others—that act through endocrine and paracrine routes to regulate glucose and lipid metabolism, insulin secretion, adipose tissue remodeling, neuroplasticity, and systemic inflammatory tone. Epigenetic modifications and exercise-responsive microRNAs further contribute to long-term metabolic reprogramming. Collectively, these molecular adaptations establish exercise as a systemic biological stimulus capable of restoring metabolic homeostasis and counteracting the pathophysiological processes underlying NCDs. Understanding these mechanisms provides a foundation for developing targeted, personalized exercise-based interventions in preventive and therapeutic medicine. Full article
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