Overexpression of Circular RNA circTTN Promotes Ferroptosis in Sepsis-Induced Cardiomyopathy

Sepsis-induced cardiomyopathy (SCM) is one of the common complications caused by sepsis. Despite the higher mortality rate associated with SCM, the pathogenesis of SCM is poorly understood. The study of circular RNA (circRNA) in a variety of diseases has accelerated over recent decades. However, the function of circRNAs in SCM is rarely reported. Here, we found that the circRNA from the TTN gene (circTTN) was increased in the SCM mouse and cell models. Modulation of circTTN affected the characteristics of SCM both in mouse and cell models. The expression of ferroptosis regulators, GPX4 and SLC7A11, in SCM models changes inversely with the level of circTTN. Function analysis revealed that circTTN promotes ferroptosis through binding to heat shock protein family A (HSPA5) protein. This finding may promote knowledge about the pathogenesis of SCM and may be helpful for targeted therapy based on circTTN in the future.