Immunoglobulin A nephropathy is a common primary glomerular disease, and its targeted therapy focuses on key links such as upstream regulation of galactose-deficient immunoglobulin A1 production, blocking immune complex deposition, inhibiting complement activation, and downstream inflammatory responses. This article systematically reviews the latest research progress of targeted therapeutic drugs based on the pathogenesis of immunoglobulin A nephropathy, summarizes their mechanisms of action and clinical research evidence, and explores the current challenges and future development directions, in order to provide references for clinical practice and research.
Immunoglobulin A nephropathy (IgAN) is an immune-mediated chronic inflammatory disease with a complex pathogenesis and diverse clinical manifestations. Currently, there is no specific treatment plan. Programmed cell death is an active and orderly way of cell death controlled by genes in the body, which maintains the homeostasis of the body and the development of organs and tissues by participating in various molecular signaling pathways. In recent years, programmed cell death has played an important regulatory role in the occurrence and development of IgAN, involving complex signaling pathways. Under pathological conditions, it may relieve kidney damage through various pathways such as reducing oxidative stress, inhibiting inflammation, and improving energy metabolism. This article provides a review of the research progress of IgAN in apoptosis, autophagy, pyroptosis, ferroptosis,and cuproptosis in order to provide new therapeutic targets for IgAN.
