Iron, oxidative stress, and metabolic dysfunction are closely linked in the development of steatotic liver disease. Excess free iron promotes the formation of reactive oxygen species (ROS), increasing oxidative stress, which is a major contributor to liver damage. Ferroptosis, an iron-dependent form of regulated cell death, is increasingly recognized as a key mechanism in liver disease progression. Iron metabolism is tightly regulated to maintain homeostasis, and disruptions in this process can lead to oxidative stress and ferroptosis, contributing to metabolic dysfunction-associated fatty liver disease (MASLD) and liver fibrosis. Iron overload is associated with increased ROS production and liver damage, and studies have shown that ferroptosis plays a role in the progression of MASLD and non-alcoholic steatohepatitis (NASH). Ferroptosis is linked to oxidative stress and lipid peroxidation, and its inhibition may offer therapeutic potential for liver diseases. Iron accumulation in the liver is associated with increased fibrosis and disease severity, and various compounds, including metformin and sorafenib, have been shown to induce or inhibit ferroptosis. Ferroptosis is also implicated in liver fibrosis and hepatocellular carcinoma (HCC), where it contributes to tissue damage and disease progression. Understanding the mechanisms of iron metabolism, oxidative stress, and ferroptosis is crucial for developing targeted therapies for liver diseases. The interplay between these processes highlights the importance of addressing iron homeostasis and oxidative stress in the treatment of metabolic liver diseases.Iron, oxidative stress, and metabolic dysfunction are closely linked in the development of steatotic liver disease. Excess free iron promotes the formation of reactive oxygen species (ROS), increasing oxidative stress, which is a major contributor to liver damage. Ferroptosis, an iron-dependent form of regulated cell death, is increasingly recognized as a key mechanism in liver disease progression. Iron metabolism is tightly regulated to maintain homeostasis, and disruptions in this process can lead to oxidative stress and ferroptosis, contributing to metabolic dysfunction-associated fatty liver disease (MASLD) and liver fibrosis. Iron overload is associated with increased ROS production and liver damage, and studies have shown that ferroptosis plays a role in the progression of MASLD and non-alcoholic steatohepatitis (NASH). Ferroptosis is linked to oxidative stress and lipid peroxidation, and its inhibition may offer therapeutic potential for liver diseases. Iron accumulation in the liver is associated with increased fibrosis and disease severity, and various compounds, including metformin and sorafenib, have been shown to induce or inhibit ferroptosis. Ferroptosis is also implicated in liver fibrosis and hepatocellular carcinoma (HCC), where it contributes to tissue damage and disease progression. Understanding the mechanisms of iron metabolism, oxidative stress, and ferroptosis is crucial for developing targeted therapies for liver diseases. The interplay between these processes highlights the importance of addressing iron homeostasis and oxidative stress in the treatment of metabolic liver diseases.