Cardiomyocyte-specific disruption of soluble epoxide hydrolase limits inflammation to preserve cardiac function
Deanna K. Sosnowski, K. Lockhart Jamieson, Artiom Gruzdev, Yingxi Li, Robert Valencia, Ala Yousef, Zamaneh Kassiri, Darryl C. Zeldin, John M. Seubert
Abstract
The cardioprotective effects of genetic disruption and pharmacological inhibition of sEH have been demonstrated in a variety of cardiac disease models, including acute LPS inflammatory injury. For the first time, it has been demonstrated that sEH genetic disruption limited to the cardiomyocyte profoundly preserves cardiac function and limits local and systemic inflammation following acute LPS exposure. Hence, cardiomyocytes serve a critical role in the innate immune response that can be modulated to protect the heart.
Topics & Concepts
Epoxide hydrolase 2InflammationInnate immune systemCardiac function curveImmune systemFunction (biology)MedicinePharmacologyImmunologyBiologyHeart failureCardiologyCell biologyEnzymeBiochemistryEicosanoids and Hypertension PharmacologyCardiovascular, Neuropeptides, and Oxidative Stress ResearchNitric Oxide and Endothelin Effects