Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia-Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling-Mediated Neutrophil Extracellular Traps Formation.

Mitigating myocardial ischemia-reperfusion (IR) injury is essential for enhancing the success of heart transplantation (HT) and improving patient outcomes. During HT, infiltrating neutrophils are influenced and regulated by various other cell types, contributing to myocardial IR injury through the excessive release of neutrophil extracellular traps (NETs). Nonetheless, the precise mechanisms underlying the interactions between neutrophils and other non-cardiomyocytes remain largely unexplored.

Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway.

Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in mitigating I/R injury. Meanwhile, verbascoside (VB), an active compound extracted from the herbaceous plant, has demonstrated myocardial protective effects.