The search for elucidating the contribution of chronic inflammation to the development of heart failure and for new treatment

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The activation of angiotensin system contributes to the development of failing heart. Chronic administration of angiotensin II (AngII) lowered cardiac ejection faraction (EF) in wild mice, however, it did not change in mice deficient of the transcription factor SREBP-1. Reactive oxygen species is involved in AngII-induced organ injury. The expression level of both the master regulator for antioxidant Nrf2, a transcription factor, and Nrf2 regulating gene for antioxidative stress was significantly decreased by AngII administration in the heart; conversely, the expression level of them did not differ in KO. Taken together, cardiac dysfunction induced by Ang II may be associated with the reduced expression of Nrf2 and its regulatory gene against antioxidative stress.