Liver fibrosis is a pathological condition marked by excessive extracellular matrix accumulation, potentially leading to cirrhosis. Macrophages play a vital role in regulating inflammatory responses, facilitating tissue repair, and orchestrating extracellular matrix remodeling through their differentiation into proinflammatory and anti‐inflammatory phenotypes. Hepatic stellate cell activation and the progression of fibrosis have been linked to ferroptosis, a controlled cell death process triggered by iron and characterized by lipid peroxidation. This review explores the interaction between ferroptosis and macrophage polarization in iron‐overload‐induced liver fibrosis. It examines how ferroptosis intensifies inflammatory and fibrotic processes through macrophage activity and identifies key macrophage marker proteins involved. Understanding this interplay offers novel therapeutic insights targeting macrophage polarization to mitigate liver fibrosis, particularly in conditions such as hemochromatosis and chronic transfusion‐dependent disorders.
Purnama et al. (Wed,) studied this question.