Abstract:

Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation, characterized by the accumulation of lipid peroxidation products, iron metabolism disorders and inactivation of antioxidant systems. It mutually amplifies inflammatory responses, forming a vicious cycle that collectively promotes the progression of diabetic kidney disease (DKD). This review systematically summarizes the core molecular mechanisms of ferroptosis and their interactions with inflammation in DKD. It outlines the bidirectional regulatory pattern whereby ferroptosis initiates inflammation and inflammatory feedback exacerbates ferroptosis. The review focuses on how key signaling pathways link ferroptosis with inflammation, analyzes their pathogenic roles and summarizes potential therapeutic strategies targeting both ferroptosis and inflammation simultaneously.

Key words:

ferroptosis, diabetic kidney disease, inflammation, signaling pathway, therapeutic strategy