The role of ferroptosis in the side effects of dexamethasone

Abstract

As a regulatory cell death caused by iron-dependent lipid peroxidation, ferroptosis is very important in the healthy development or disease progression of various organisms. Dexamethasone is a glucocorticoid with vigorous immunosuppressive activity and anti-inflammatory effects. On the other hand, it can cause some side effects under long-term or high-dose administration, including secondary osteoporosis and osteonecrosis, which are associated with the elevated autophagy and involvement of ferroptosis. Autophagy, an intracellular degradation system, plays a crucial role in ferroptosis. It has been increasingly proved that ferroptosis is potentially related to the dexamethasone-induced side effects, in which autophagy may be involved. However, the regulatory mechanism of ferroptosis in the dexamethasone-induced side effects is unclear. This review summarizes the molecular mechanisms of ferroptosis, the dexamethasone-induced side effects, and the potential relationships between ferroptosis and dexamethasone-induced side effects, aiming to provide novel insight into the interplay between them.

Keywords

• ferroptosis
• dexamethasone
• autophagy
• glucocorticoids
• dexamethasone-induced side effects