Redox Regulation of Soluble Epoxide Hydrolase-Implications for Cardiovascular Health and Disease

Cell responses to changes in their redox state are significantly mediated by reversible oxido-reductive post-translational modifications of proteins, potentially altering their activities or interactions. These modifications are important for the homeostatic responses of cells to environmental changes that alter their redox state. Such redox regulatory mechanisms not only operate to maintain health, but can become dysregulated and contribute to pathophysiology. In this review, we focus on the redox control of soluble epoxide hydrolase (sEH), which is widely expressed, including in blood vessels and cardiomyocytes. We review the different types of oxidative modifications that regulate sEH and how they may alter cardiovascular physiology and affect disease progression during stress.

Automated summary

Cell responses to changes in redox state are mediated by reversible protein modifications, which can alter protein activities or interactions. These modifications are crucial for cells' homeostatic responses to environmental changes in redox state. The dysregulation of these redox regulatory mechanisms can contribute to pathophysiology. This review focuses on the redox control of soluble epoxide hydrolase (sEH), its different oxidative modifications, and their impact on cardiovascular physiology and disease progression during stress.