Sepsis is a systemic disease with severe health consequences, and it was redefined in 2016 as a life-threatening organ dysfunction caused by an abnormal host response to infection and is a global public health priority. In recent years, there has been increasing recognition of the role of dysregulated micronutrient iron metabolism in the pathogenesis of sepsis. The concept of ferroptosis, an iron-dependent, non-apoptotic mode of cell death characterized by the accumulation of lipid reactive oxygen species (ROS), was first proposed by Dixon et al. in 2012. As a novel mode of programmed cell death, ferroptosis differs in morphological and biochemical characteristics from various forms of cell death, such as apoptosis, autophagy, necrosis and lysis. Recent studies have shown that ferroptosis plays an important regulatory role in the development of sepsis and has become a research focus and highlight for the diagnosis and prognosis of related diseases. Therefore, this paper reviews the latest developments in ferroptosis in sepsis, in order to further understanding its pathogenesis and providing new therapeutic targets for sepsis-related organ dysfunction.