Post-Translational Modification of GPX4 is a Promising Target for Treating Ferroptosis-Related Diseases
Glutathione peroxidase 4 (GPX4) is among the most significant antioxidant enzymes. Because the key regulator of ferroptosis, GPX4 has attracted considerable attention within the fields of cancer, cardiovascular, and neuroscience research previously ten years. How you can regulate GPX4 activity has turned into a hot subject nowadays. GPX4 protein level is controlled transcriptionally by transcription factor SP2 or Nrf2. GPX4 activity could be upregulated by supplementing intracellular selenium or glutathione, as well as be inhibited by ferroptosis inducers for example ML162 and RSL3. These ML162 regulatory mechanisms of GPX4 level/activity have previously proven an excellent possibility of treating ferroptosis-related illnesses in preclinical studies, particularly in cancer cells. Until lately, research reveal that GPX4 can undergo publish-translational modifications (PTMs), for example ubiquitination, succination, phosphorylation, and glycosylation. PTMs of GPX4 modify the protein level/activity of GPX4, indicating that modifying these processes could be a potential therapy for the treatment of ferroptosis-related illnesses. This ML162 short article summarizes the protein characteristics, enzyme qualities, and PTMs of GPX4. Additionally, it supplies a hypothetical idea for the treatment of ferroptosis-related illnesses by individuals PTMs of GPX4.