Oxidative Stress: Signaling Pathways, Biological Functions, and Disease

Area of Science:

• Biochemistry and Molecular Biology
• Pathophysiology
• Systems Biology

Background:

• Dysregulated reactive oxygen species (ROS) and reactive nitrogen species accumulation disrupts redox homeostasis, leading to oxidative stress (OS).
• OS contributes to disease progression by modulating signaling pathways, inflammation, mitochondrial function, metabolic homeostasis, and autophagy.
• Previous research has primarily focused on OS in single-organ diseases, neglecting its systemic role in pan-organ diseases and interorgan communication.

Purpose of the Study:

• To integrate multidisciplinary evidence elucidating the biological functions of OS in cellular signaling, homeostasis, and cross-organ crosstalk.
• To systematically dissect OS-driven molecular mechanisms and pathophysiological networks across 10 major organ systems.
• To critically examine OS-related therapeutic targets and explore synergistic redox-based therapeutic strategies.

Main Methods:

• Systematic review and integration of multidisciplinary evidence.
• Dissection of OS-driven molecular mechanisms and pathophysiological networks.
• Critical examination of therapeutic targets and strategies.

Main Results:

• OS impacts cellular signaling, homeostasis, and interorgan communication.
• OS-driven molecular mechanisms and pathophysiological networks identified across 10 major organ systems.
• Potential therapeutic targets, including antioxidants and ROS-generating enzymes, and synergistic strategies were examined.

Conclusions:

• A holistic framework for understanding the systemic impact of OS beyond single-organ paradigms is established.
• Novel insights into disease mechanisms and therapeutic innovations for OS-driven diseases are provided.
• The review lays the foundation for precision medicine approaches to mitigate OS and improve multiorgan health.