Reactive Oxygen Species-Mediated Mitochondrial-Targeted Therapeutics in Hepatic Disorders: Current Progress and Future Opportunities

Abstract

Reactive oxygen species (ROS) are key mediators of mitochondrial dysfunction, contributing to the onset and development of hepatic disorders, including nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and liver fibrosis. Mitochondria, as central regulators of cellular energy and metabolism, are both sources and targets of ROS, making them critical in understanding liver disease pathology. Current approaches include the development of mitochondria-specific antioxidants, therapeutic agents that enhance mitochondrial biogenesis, and nanotechnology-based delivery systems to improve precision targeting. Emerging approaches such as the modulation of mitochondrial dynamics and mitophagy hold significant potential to restore mitochondrial function and cellular homeostasis. The various causes of mitochondrial dysfunction, with a focus on ROS involvement in the pathogenesis of hepatic disorders, are discussed. Here, currently explored therapeutic remedies for mitochondrial dysfunction and their potential in translating them into clinical applications are covered. A discussion of recent advances in mitochondrial-targeted therapeutics for hepatic disorders is also included. The review concludes by identifying promising directions for future research, emphasizing the need for innovative strategies to exploit the interplay between ROS and mitochondrial dysfunction. These advances could pave the way for targeted, effective therapies for managing hepatic disorders.