مشخصات پژوهش

The increasing prevalence of Non-Alcoholic Fatty Liver Disease (NAFLD) necessitates a deeper understanding of its underlying mechanisms, particularly the role of oxidative stress and mitochondrial dysfunction. As a leading cause of chronic liver disease worldwide, NAFLD not only imposes a significant public health burden but also presents escalating healthcare costs due to its complications, including cirrhosis and liver cancer. Thus, addressing the factors contributing to NAFLD is critical for enhancing patient outcomes and reducing the future burden on healthcare systems. Investigating the link between oxidative stress and mitochondrial function is particularly important for several reasons. First, oxidative stress is a defining feature of NAFLD and has been shown to exacerbate metabolic dysfunction, leading to a vicious cycle of liver damage. Understanding how oxidative stress affects mitochondrial integrity and function can elucidate key pathways involved in disease progression. This knowledge is essential for the identification of early biomarkers that can aid in the diagnosis and monitoring of NAFLD. Second, mitochondrial dysfunction is central to the pathology of NAFLD and may provide actionable insights for therapeutic intervention. By identifying the specific mechanisms through which oxidative stress impairs mitochondrial function, potential treatment strategies, including antioxidant therapies or drugs that target mitochondrial dynamics, may be developed. These interventions could not only halt disease progression but also reverse damage at an early stage, significantly altering the disease trajectory for affected individuals. Lastly, this research topic holds the promise of filling critical gaps in the current knowledge base, paving the way for future studies aimed at integrating oxidative stress and mitochondrial function into comprehensive NAFLD management protocols. By advancing our understanding of these interrelated processes, we can contribute to th