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Oxidative-Stress in Human Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 241

Special Issue Editor


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Guest Editor
Versiti Blood Research Institute, P.O. Box 2178, Milwaukee, WI 53201-2178, USA
Interests: cardiovascular disorders; metabolic disorders; oxidative stress; endothelial Rap1 signaling; nitric oxide regulation; diabetic cardiomyopathy

Special Issue Information

Dear Colleagues,

Oxidative stress, defined as an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant defenses, is increasingly recognized as a central mechanism in the pathophysiology of numerous human diseases. While physiological ROS generation is indispensable for redox signaling, host defense, and metabolic adaptation, sustained or excessive accumulation disrupts protein folding, lipid integrity, nucleic acid stability, and redox-sensitive pathways. This duality highlights its complex role in health and disease.

A growing body of evidence implicates oxidative stress in the onset and progression of cardiovascular diseases, neurodegeneration, metabolic disorders, cancer, and chronic inflammatory conditions. Furthermore, lifestyle and environmental factors, including diet, smoking, pollutants, and aging modulate oxidative homeostasis, thereby influencing disease susceptibility and outcomes. Advances in molecular biology and clinical research have uncovered mechanistic links between oxidative stress and endothelial dysfunction, mitochondrial impairment, and immune dysregulation. Novel biomarkers, imaging modalities, and therapeutic approaches, including pharmacological antioxidants, nutraceuticals, and redox-targeted interventions, are reshaping our understanding of oxidative stress in translational and clinical contexts.

This Special Issue will provide an interdisciplinary platform for the latest insights into oxidative stress in human health and disease. We invite contributions exploring molecular mechanisms, methodological innovations, clinical implications, and novel therapeutic strategies, spanning fields such as biochemistry, pharmacology, nutrition, and precision medicine. By integrating basic and clinical perspectives, this Special Issue will deepen our understanding of oxidative stress as a biological phenomenon and highlight opportunities for therapeutic intervention to improve human health.

Dr. Ramoji Kosuru
Guest Editor

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Keywords

  • oxidative stress
  • ROS
  • redox signaling
  • metabolic adaptation
  • oxidative homeostasis
  • endothelial dysfunction

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Published Papers (1 paper)

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Review

25 pages, 4500 KB  
Review
Integrating Senescence and Oxidative Stress in Cardiac Disease
by Hyeong Rok Yun, Manish Kumar Singh, Sunhee Han, Jyotsna S. Ranbhise, Joohun Ha, Sung Soo Kim and Insug Kang
Int. J. Mol. Sci. 2025, 26(24), 11917; https://doi.org/10.3390/ijms262411917 - 10 Dec 2025
Abstract
Cellular senescence and oxidative stress constitute an interdependent axis that underlies cardiac pathophysiology. Cellular senescence, defined as durable proliferative arrest, is initiated and sustained by redox imbalance, whereas mitochondrial reactive oxygen species function as signaling molecules or mediators of injury. In the heart, [...] Read more.
Cellular senescence and oxidative stress constitute an interdependent axis that underlies cardiac pathophysiology. Cellular senescence, defined as durable proliferative arrest, is initiated and sustained by redox imbalance, whereas mitochondrial reactive oxygen species function as signaling molecules or mediators of injury. In the heart, cellular senescence and oxidative stress influence remodeling and dysfunction across diseases, including ischemia–reperfusion injury, heart failure with preserved ejection fraction, dilated cardiomyopathy, and cardiac hypertrophy. Accordingly, delineating stress adaptation in cellular senescence is essential for elucidating oxidative stress-related pathogenesis. In this review, we attempt to provide an overview of the fundamental mechanisms and functions of cellular senescence in response to oxidative stress and redox signaling in disease. In addition, we integrate experimental and clinical evidence and delineate implications for mechanism-informed prevention and therapy. Full article
(This article belongs to the Special Issue Oxidative-Stress in Human Health and Diseases)
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