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As a common and frequently occurring disease, heart failure has been paid more and more attention, but the mechanism of its occurrence and development is still unclear. This study investigated that PGAM5 expression levels in heart failure and its underlying mechanisms in vivo and in vitro. The inhibition of PGAM5 mRNA expression levels in patients with heart failure was compared with the normal group. The serum of PGAM5 mRNA expression was negative correlation with collagen I and collagen III in patients with heart failure. PGAM5 mRNA and protein expression in the heart tissue of mice with heart failure were down-regulated at a time-dependent rate. The inhibition of PGAM5 presented heart failure in the model. PGAM5 reduced inflammation and inhibited ROS-induced oxidative stress in models of heart failure. PGAM5 reduced Ferroptosis in models of heart failure. PGAM5 regulated Keap1/Nrf2 signaling pathway. IP also showed that PGAM5 protein combined with the Keap1 protein. PGAM5 could increase Keap1 protein ubiquitination. Keap1 inhibition affected the effects of PGAM5 in model of heart failure. We conclude that the protection of PGAM5 reduced ROS-induced oxidative stress and ferroptosis by the Keap1/Nrf2 signaling pathway in heart failure, suggesting that targeting this mechanism of PGAM5 may be a feasible strategy to treat heart failure.

PGAM5 expression levels in heart failure and protection ROS-induced oxidative stress and ferroptosis by Keap1/Nrf2