Ferroptosis is a newly identified form of cell death that has garnered attention in recent years. Current research has clarified several key mechanisms of ferroptosis, with reactive oxygen species, oxidative stress, and iron me tabolism emerging as central factors. Additionally, various signaling pathways, molecules, and organelles also contribute to the regulation and progression of ferroptosis. Activation of ferroptosis has significant implications for sepsis-related inflammation, providing both a valuable area for scientific investigation and a potential target for therapeutic interventions. This article reviews the biological processes and molecular mechanisms of ferroptosis, as well as the small molecules and signaling pathways that regulate it. Additionally, we discuss the role of ferropto sis in the progression of sepsis and its contribution to organ damage.
Keywords: Ferroptosis, sepsis, inflammation, GPX4