Erectile dysfunction (ED) is a common sexual dysfunction in men that can occur with the onset of sexual activity or even earlier, and the development of ED involves a variety of pathophysiologic mechanisms. Organic erectile dysfunction refers to a type of erectile dysfunction that is primarily caused by physical or organic factors rather than psychological or emotional factors. Worldwide, the incidence and prevalence of ED are high. Currently, the mainstay of ED treatment is the use of medications such as phosphodiesterase type 5 inhibitors (PDE5Is). However, these medications cause adverse effects such as flushing, indigestion and headaches and are not effective for some ED patients. Therefore, there is an urgent need to explore new targets of action for the treatment of ED. Ferroptosis is a type of iron-dependent regulated cell death initiated by lipid peroxidation and is a novel form of programmed cell death associated with the pathogenesis of various diseases. Prior research has provided evidence that the ferroptosis pathway plays a pivotal role in the modulation of ED, establishing this pathway as a significant foundation for the development of potential therapeutic interventions for ED. Experiments have shown that the inhibition of ferroptosis can improve ED. This article systematically introduces the role and influence of ferroptosis in various types of organic erectile dysfunction and describes the molecular mechanism, related pathways, and potential targets, providing a theoretical basis for the clinical diagnosis and treatment of ED.
Keywords: GPX4; erectile dysfunction; ferroptosis.
© 2023 The Author(s).