Dwi Widyawati
Department Of Physiology, Faculty Of Medicine And Health Science, Sultan Ageng Tirtayasa University, Banten 42118, Indonesia

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Targeting Hypoxia-Induced Oxidative Stress via Natural Antioxidant Modulation: From Cellular Signaling to Therapeutic Perspectives Dwi Widyawati; Ghea Farmaning Thias Putri; Rifdah Hanifah; Firda Asmaul Husna; Nabila Aulia Tsaqifah; Ainina Al Shadrina
International Journal of Cell and Biomedical Science Vol 4 No 12 (2025)
Publisher : Stem Cell and Cancer Research (SCCR)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59278/cbs.v4i12.76

Abstract

Hypoxia is a fundamental physiological and pathological condition that disrupts cellular homeostasis through the excessive generation of reactive oxygen species (ROS), leading to oxidative stress, inflammation, and organ dysfunction. The imbalance between ROS production and antioxidant defense mechanisms is a key contributor to cell injury and disease progression. This review aims to elucidate the molecular interactions among major redox-sensitive signaling pathways hypoxia-inducible factor 1 (HIF-1), nuclear factor kappa B (NF-κB), and nuclear factor erythroid 2-related factor 2 (Nrf2) in hypoxia-induced oxidative stress, and to highlight the therapeutic potential of natural antioxidants in modulating these pathways. Relevant literature published over the past five years (2020-2025) was systematically reviewed using databases including PubMed, Scopus, and ScienceDirect. The selected studies focused on molecular redox signaling, hypoxia-induced oxidative mechanisms, and the modulatory roles of natural phytochemicals such as Ficus carica bioactive compounds. Recent findings reveal that natural antioxidants regulate redox signaling by activating Nrf2-dependent antioxidant responses, suppressing NF-κB driven inflammation, and stabilizing HIF-1α under hypoxic conditions. Phytochemicals, particularly flavonoids and polyphenols, exhibit strong potential to restore oxidative balance, protect cellular integrity, and reduce hypoxia-induced damage. Modulating hypoxia-induced oxidative stress through natural antioxidant pathways offers a promising therapeutic strategy. A deeper understanding of the molecular crosstalk between redox signaling and phytochemical activity may provide new insights for developing preventive and therapeutic interventions against hypoxia-related disorders.
Maternal Obesity, Metabolic Syndrome, and Long-Term Effects on Offspring: A Developmental Origins of Health and Disease (DOHaD) Perspective Tsaqifah, Nabila Aulia; Hanifah, Rifdah; Husna, Firda Asma'ul; Hidayati, Mailani Dwi; Widyawati , Dwi; Putri, Ghea Farmaning Thias; Al Shadrina, Ainina
Nusantara Medical Science Journal Vol. 10 No. 2 (2025): Volume 10 Issue 2, July - December 2025
Publisher : Faculty of Medicine, Hasanuddin University.

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20956/nmsj.v10i2.47907

Abstract

Introduction: The global prevalence of obesity among women of reproductive age has increased markedly over the past two decades, reaching 24% in high-income and 16% in low- and middle-income countries. This trend contributes to adverse maternal and neonatal outcomes, including a 2–4-fold higher risk of gestational diabetes, a threefold increase in preeclampsia, and up to a 50% higher caesarean delivery rate. Maternal metabolic disorders also have long-term consequences for offspring metabolic and cardiovascular health. Objective: To synthesize current biological and epidemiological evidence linking maternal metabolic status to offspring health within the Developmental Origins of Health and Disease (DOHaD) framework. Methods: A comprehensive search was conducted in PubMed, Scopus, and Web of Science from January 2015 to September 2025 using keywords related to maternal obesity, metabolic syndrome, DOHaD, offspring health, and epigenetics. Included studies comprised human and animal research with follow-up beyond two years, while case reports, editorials, and studies without long-term outcomes were excluded. Findings: From 22 eligible studies, consistent evidence indicates that maternal obesity and metabolic syndrome affect offspring through placental dysfunction, systemic inflammation, and epigenetic reprogramming. Offspring of obese mothers show a 1.5–2.8-fold increased risk of obesity and insulin resistance during adolescence and adulthood. Epigenome-wide analyses reveal altered methylation of genes regulating lipid metabolism (LEP, IGF2) and inflammatory pathways, supporting the DOHaD hypothesis. Conclusion: Maternal metabolic health critically shapes offspring developmental and metabolic outcomes. Preconception and antenatal interventions targeting metabolic optimization provide key opportunities to prevent intergenerational transmission of metabolic risk and promote healthier future generations.