The article "The emerging role of oxidative stress in inflammatory bowel disease" by Muro et al. explores the significant role of oxidative stress in the development and progression of inflammatory bowel disease (IBD). IBD, characterized by chronic immune responses affecting the digestive system, includes Crohn's disease (CD) and ulcerative colitis (UC). The prevalence of IBD has been increasing, particularly in Asia, and its exact cause remains unknown, involving genetic, environmental, and immunological factors. Treatment options are evolving, including targeted therapies, personalized medicine, biologics, stem cell therapies, and fecal microbiota transplantation. Oxidative stress, defined as an imbalance between oxidants and antioxidants, plays a crucial role in IBD. It involves the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to cellular damage and immune system activation. ROS can damage biomolecules such as lipids, proteins, and DNA, disrupting cellular functions and contributing to inflammation. RNS, particularly nitric oxide (NO), can form peroxynitrite (ONOO-), which further exacerbates oxidative stress. The article discusses the mechanisms by which oxidative stress contributes to IBD, including the overproduction of ROS, damage to biomolecules, mitochondrial dysfunction, immune cell recruitment, impaired antioxidant defense, and activation of inflammatory pathways. Key transcription factors like Nrf2 and NF-κB are involved in regulating the response to oxidative stress and inflammation. Targeting oxidative stress through antioxidant therapies is a promising approach to managing IBD. The article highlights the potential of targeting specific pathways, such as the TLR4/NF-κB and Nrf2-ARE pathways, to reduce inflammation and enhance antioxidant defenses. Additionally, the role of cytokines and signal pathways, such as MAPK and PI3K/Akt, in the pathophysiology of IBD is discussed, suggesting potential therapeutic targets. Overall, the article emphasizes the importance of understanding oxidative stress in IBD and the potential of targeting these pathways to develop more effective treatments.The article "The emerging role of oxidative stress in inflammatory bowel disease" by Muro et al. explores the significant role of oxidative stress in the development and progression of inflammatory bowel disease (IBD). IBD, characterized by chronic immune responses affecting the digestive system, includes Crohn's disease (CD) and ulcerative colitis (UC). The prevalence of IBD has been increasing, particularly in Asia, and its exact cause remains unknown, involving genetic, environmental, and immunological factors. Treatment options are evolving, including targeted therapies, personalized medicine, biologics, stem cell therapies, and fecal microbiota transplantation. Oxidative stress, defined as an imbalance between oxidants and antioxidants, plays a crucial role in IBD. It involves the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to cellular damage and immune system activation. ROS can damage biomolecules such as lipids, proteins, and DNA, disrupting cellular functions and contributing to inflammation. RNS, particularly nitric oxide (NO), can form peroxynitrite (ONOO-), which further exacerbates oxidative stress. The article discusses the mechanisms by which oxidative stress contributes to IBD, including the overproduction of ROS, damage to biomolecules, mitochondrial dysfunction, immune cell recruitment, impaired antioxidant defense, and activation of inflammatory pathways. Key transcription factors like Nrf2 and NF-κB are involved in regulating the response to oxidative stress and inflammation. Targeting oxidative stress through antioxidant therapies is a promising approach to managing IBD. The article highlights the potential of targeting specific pathways, such as the TLR4/NF-κB and Nrf2-ARE pathways, to reduce inflammation and enhance antioxidant defenses. Additionally, the role of cytokines and signal pathways, such as MAPK and PI3K/Akt, in the pathophysiology of IBD is discussed, suggesting potential therapeutic targets. Overall, the article emphasizes the importance of understanding oxidative stress in IBD and the potential of targeting these pathways to develop more effective treatments.