Institute for Heart Research, Centre of Experimental Medicine Slovak Academy of Sciences, Bratislava, Slovak republic.
Physiol Res. 2023 Jun 9;72(S1):S61-S72. doi: 10.33549/physiolres.935112.
Iron is an essential mineral participating in numerous biological processes in the organism under physiological conditions. However, it may be also involved in the pathological mechanisms activated in various cardiovascular diseases including myocardial ischemia/reperfusion (I/R) injury, due to its involvement in reactive oxygen species (ROS) production. Furthermore, iron has been reported to participate in the mechanisms of iron-dependent cell death defined as "ferroptosis". On the other hand, iron may be also involved in the adaptive processes of ischemic preconditioning (IPC). This study aimed to elucidate whether small amounts of iron may modify the cardiac response to I/R in isolated perfused rat hearts and their protection by IPC. Pretreatment of the hearts with iron nanoparticles 15 min prior to sustained ischemia (iron preconditioning, Fe-PC) did not attenuate post-I/R contractile dysfunction. Recovery of left ventricular developed pressure (LVDP) was significantly improved only in the group with combined pretreatment with iron and IPC. Similarly, the rates of contraction and relaxation [+/-(dP/dt)max] were almost completely restored in the group preconditioned with a combination of iron and IPC but not with iron alone. In addition, the severity of reperfusion arrhythmias was reduced only in the iron+IPC group. No changes in protein levels of "survival" kinases of the RISK pathway (Reperfusion Injury Salvage Kinase) were found except for reduced caspase 3 levels in both preconditioned groups. The results indicate that a failure to precondition rat hearts with iron may be associated with the absent upregulation of RISK proteins and the pro-ferroptotic effect manifested by reduced glutathione peroxidase 4 (GPX4) levels. However, combination with IPC suppressed the negative effects of iron resulting in cardioprotection.
铁是一种必需的矿物质,参与生物体的许多生理过程。然而,由于其参与活性氧(ROS)的产生,它也可能参与各种心血管疾病的病理机制,包括心肌缺血/再灌注(I/R)损伤。此外,据报道,铁参与了定义为“铁死亡”的铁依赖性细胞死亡机制。另一方面,铁也可能参与缺血预处理(IPC)的适应过程。本研究旨在阐明少量铁是否可以改变分离灌注大鼠心脏对 I/R 的心脏反应及其对 IPC 的保护作用。在持续缺血前 15 分钟用铁纳米颗粒预处理心脏(铁预处理,Fe-PC)不会减轻 I/R 后收缩功能障碍。只有在铁和 IPC 联合预处理的组中,左心室发展压(LVDP)的恢复明显改善。同样,在铁和 IPC 联合预处理的组中,收缩和舒张速度[+/-(dP/dt)max]几乎完全恢复,但单独用铁预处理的组则没有。此外,只有在铁+IPC 组中,再灌注心律失常的严重程度才降低。除了两个预处理组中 caspase 3 水平降低外,RISK 通路(再灌注损伤挽救激酶)的“存活”激酶的蛋白水平没有变化。结果表明,铁预处理大鼠心脏失败可能与 RISK 蛋白的上调缺失以及谷胱甘肽过氧化物酶 4(GPX4)水平降低导致的促铁死亡作用有关。然而,与 IPC 联合使用可抑制铁的负面作用,从而实现心脏保护。