In a new study, Assistant Professor of Molecular and Integrative Physiology Kevin Xiang and colleagues show that the PGE2 stimulation attenuates the adrenergic-induced cardiac contractile response in animal hearts.
Inflammation is a well-known independent risk factor for cardiovascular diseases, including atherosclerosis and heart failure. Anti-inflammation drugs such as aspirin and ibuprofen show significant benefits for patients in preventing cardiovascular diseases. However, how inflammation contributes to development of these diseases is still largely unknown.
Prostaglandin E is a major proinflammatory factor whose level is elevated in the blood and myocardium. In a new study in PNAS, Assistant Professor of Molecular and Integrative Physiology Kevin Xiang and colleagues determine whether inflammatory factor prostaglandin E2-induced signaling directly modulates adrenergic stimulation of cardiac contractility by adrenolines. Their study reveals that prostaglandin E2 can directly impair the adrenergic regulation of myocardium contraction via an elegant intracellular interaction. These studies provide a novel understanding of how inflammatory factor prostaglandin E directly affects heart function, and contributes to the development of heart diseases. Since most non-steroidal anti-inflammatory drugs (NSAID, including ibuprofen) reduce the levels of prostaglandin E2 by inhibiting an enzyme Cox2, this study may also explain how these anti-inflammatory drugs could help prevent cardiac diseases.
According to Professor Xiang, "This study really pinpoints the action of inflammation on the function of animal hearts, which provides a direction on how we access the impact of inflammation on heart function, and illuminates potentially new strategies in preventing and treating heart failure in patients."