Role of the Ubiquitin-Proteasome System in Ferroptosis

Ferroptosis is a new type of regulated cell death caused by iron dependent lipid peroxidation. Growing evidences indicate that ferroptosis plays an important role in the occurrence and development of various diseases including tumor. Therefore, how to treat diseases by regulating ferroptosis has become a major direction of basic and clinical research. The UPS (ubiquitin-proteasome system) is the main degradation pathway of eukaryotic proteins. Ub (ubiquitin) is conjugated to proteins that should be degraded, and then the proteasome recognizes and degrades them. Dysfunction of the ubiquitin-proteasome pathway leads to a variety of pathological processes, thus maintain the stability of its biological functions is of great significance. Regulation of protein stability is a crucial part of the complex molecular mechanism of ferroptosis, and the ubiquitin-proteasome system, as a key regulatory system of macromolecular homeostasis in eukaryotes, can directly or indirectly affect ferroptosis by regulating related molecules or related signaling pathways. To provide a reference for the treatment of diseases targeting ferroptosis, this article review the related molecules or signaling pathways involved in the regulation of ferroptosis by the ubiquitin proteasome system.

CSTR: 32200.14.cjcb.2023.01.0018