El-Sehrawy Amr Ali Mohamed Abdelgawwad, Mohammed Abdulsalam Najm, Gupta Jitendra, Mohammed Jaafaru Sani, Roopashree R, Kashyap Aditya, Janney J Bethanney, Sahoo Samir, Al-Hasnaawei Shaker, Nasr Yassir Mohammed
Internal Medicine, Diabetes, Endocrinology and Metabolism, Mansoura University, Mansoura, Egypt.
Department of Medical Laboratory Techniques, College of Health and Technology, University of Al-Maarif, Ramadi, Al-Anbar 31001, Iraq.
Pathol Res Pract. 2025 Aug;272:156053. doi: 10.1016/j.prp.2025.156053. Epub 2025 May 30.
Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder with a growing global impact, closely linked to metabolic syndrome and lifestyle factors. Oxidative stress, arising from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a pivotal role in the pathogenesis of NAFLD. It drives lipid peroxidation, mitochondrial dysfunction, and inflammatory cascades, exacerbating hepatic steatosis and promoting progression to non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. This review delves into the molecular mechanisms of oxidative stress in NAFLD, highlighting its contribution to disease initiation and progression. It explores key sources of ROS, such as mitochondrial dysfunction, and discusses the interplay between oxidative stress, insulin resistance, and inflammation. Strategies to mitigate oxidative damage, including lifestyle modifications, dietary antioxidants, and emerging pharmacological interventions, are examined with a focus on their therapeutic potential. By unraveling the oxidative stress pathways in NAFLD, this review aims to provide insights into effective preventive measures and therapeutic approaches. Understanding these mechanisms offers a foundation for future research and clinical innovations to combat the burden of NAFLD and its complications.
非酒精性脂肪性肝病(NAFLD)是一种普遍存在的肝脏疾病,在全球的影响日益增大,与代谢综合征和生活方式因素密切相关。氧化应激源于活性氧(ROS)生成与抗氧化防御之间的失衡,在NAFLD的发病机制中起关键作用。它会引发脂质过氧化、线粒体功能障碍和炎症级联反应,加剧肝脏脂肪变性,并促使疾病进展为非酒精性脂肪性肝炎(NASH)、纤维化和肝硬化。本综述深入探讨了NAFLD中氧化应激的分子机制,强调了其对疾病起始和进展的作用。它探究了ROS的关键来源,如线粒体功能障碍,并讨论了氧化应激、胰岛素抵抗和炎症之间的相互作用。研究了减轻氧化损伤的策略,包括生活方式改变、膳食抗氧化剂和新兴的药物干预措施,并重点关注了它们的治疗潜力。通过揭示NAFLD中的氧化应激途径,本综述旨在为有效的预防措施和治疗方法提供见解。了解这些机制为未来对抗NAFLD及其并发症负担的研究和临床创新奠定了基础。