Abstract:Ferroptosis is a form of cell death characterized by iron-dependent lipid peroxidation and the accumulation of reactive oxygen species, distinct from apoptosis and other forms of cell death. Inflammation is the body’s defense response to stimuli, manifested as redness, swelling, heat, pain, and dysfunction, and an imbalance in the inflammatory response can lead to immune system dysregulation, cellular dysfunction, and death. Increasing researches suggest that the activation of inflammation, including the activation of various inflammation-related signaling pathways, can lead to ferroptosis. This review will focus on the classical inflammatory pathways, including the mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathways, and elucidate their roles in ferroptosis, discussing their potential mechanisms in the occurrence of diseases associated with ferroptosis, which contributes to a better understanding of the pathophysiological processes of ferroptosis.