29 March 2024 | Jinghua Bu, Yanbo Liu, Rongrong Zhang, Sijie Lin, Jingbin Zhuang, Le Sun, Lingyu Zhang, Hui He, Rongrong Zong, Yang Wu and Wei Li
Oxidative stress is a key factor in the development of dry eye disease (DED). This review highlights the role of reactive oxygen species (ROS) in the pathogenesis of DED, emphasizing the importance of antioxidant strategies in its treatment. DED is a multifactorial condition characterized by tear film instability, ocular surface damage, and inflammation. Oxidative stress arises when ROS production exceeds the capacity of the antioxidant defense system, leading to cellular apoptosis and further oxidative damage. This exacerbates inflammation and cellular stress, creating a vicious cycle of oxidative stress in DED. Antioxidants have emerged as a novel therapeutic approach for DED, as they can break this cycle by reducing ROS levels and mitigating oxidative damage.
Oxidative stress is closely linked to DED, with increased ROS production and reduced antioxidant capacity observed in DED patients. Factors such as aging, lifestyle, and environmental exposure contribute to oxidative stress, which in turn leads to ocular surface damage and inflammation. Animal and in vitro studies have shown that oxidative stress plays a significant role in the progression of DED, with various models demonstrating the effects of oxidative stress on tear film stability, corneal epithelial damage, and inflammatory responses.
Clinical studies have also confirmed the association between oxidative stress and DED, with biomarkers such as 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) indicating increased oxidative damage in DED patients. These biomarkers can be used to assess disease severity and monitor treatment effectiveness. Antioxidants such as lactoferrin, N-acetylcysteine (NAC), and SkQ1 have shown promise in reducing oxidative stress and improving DED symptoms. Additionally, various plant extracts and compounds have demonstrated antioxidant properties that may help alleviate DED symptoms by reducing oxidative stress.
Future research should focus on developing innovative therapeutic strategies that target oxidative stress in DED. This includes exploring the use of antioxidants in clinical settings, improving the efficacy of existing treatments, and understanding the complex interplay between oxidative stress and other factors in DED. The findings from this review provide a foundation for further research into the role of oxidative stress in DED and the development of new therapeutic approaches for this complex ocular disorder.Oxidative stress is a key factor in the development of dry eye disease (DED). This review highlights the role of reactive oxygen species (ROS) in the pathogenesis of DED, emphasizing the importance of antioxidant strategies in its treatment. DED is a multifactorial condition characterized by tear film instability, ocular surface damage, and inflammation. Oxidative stress arises when ROS production exceeds the capacity of the antioxidant defense system, leading to cellular apoptosis and further oxidative damage. This exacerbates inflammation and cellular stress, creating a vicious cycle of oxidative stress in DED. Antioxidants have emerged as a novel therapeutic approach for DED, as they can break this cycle by reducing ROS levels and mitigating oxidative damage.
Oxidative stress is closely linked to DED, with increased ROS production and reduced antioxidant capacity observed in DED patients. Factors such as aging, lifestyle, and environmental exposure contribute to oxidative stress, which in turn leads to ocular surface damage and inflammation. Animal and in vitro studies have shown that oxidative stress plays a significant role in the progression of DED, with various models demonstrating the effects of oxidative stress on tear film stability, corneal epithelial damage, and inflammatory responses.
Clinical studies have also confirmed the association between oxidative stress and DED, with biomarkers such as 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) indicating increased oxidative damage in DED patients. These biomarkers can be used to assess disease severity and monitor treatment effectiveness. Antioxidants such as lactoferrin, N-acetylcysteine (NAC), and SkQ1 have shown promise in reducing oxidative stress and improving DED symptoms. Additionally, various plant extracts and compounds have demonstrated antioxidant properties that may help alleviate DED symptoms by reducing oxidative stress.
Future research should focus on developing innovative therapeutic strategies that target oxidative stress in DED. This includes exploring the use of antioxidants in clinical settings, improving the efficacy of existing treatments, and understanding the complex interplay between oxidative stress and other factors in DED. The findings from this review provide a foundation for further research into the role of oxidative stress in DED and the development of new therapeutic approaches for this complex ocular disorder.