Punziano Carolina, Trombetti Silvia, Cesaro Elena, Grosso Michela, Faraonio Raffaella
Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, 80131 Naples, Italy.
Department of Veterinary Medicine and Animal Productions, University of Naples Federico II, 80137 Naples, Italy.
Antioxidants (Basel). 2024 Feb 28;13(3):298. doi: 10.3390/antiox13030298.
Ferroptosis is a type of programmed cell death that differs from apoptosis, autophagy, and necrosis and is related to several physio-pathological processes, including tumorigenesis, neurodegeneration, senescence, blood diseases, kidney disorders, and ischemia-reperfusion injuries. Ferroptosis is linked to iron accumulation, eliciting dysfunction of antioxidant systems, which favor the production of lipid peroxides, cell membrane damage, and ultimately, cell death. Thus, signaling pathways evoking ferroptosis are strongly associated with those protecting cells against iron excess and/or lipid-derived ROS. Here, we discuss the interaction between the metabolic pathways of ferroptosis and antioxidant systems, with a particular focus on transcription factors implicated in the regulation of ferroptosis, either as triggers of lipid peroxidation or as ferroptosis antioxidant defense pathways.
铁死亡是一种程序性细胞死亡，不同于凋亡、自噬和坏死，并且与多种生理病理过程相关，包括肿瘤发生、神经退行性变、衰老、血液疾病、肾脏疾病以及缺血再灌注损伤。铁死亡与铁蓄积有关，引发抗氧化系统功能障碍，这有利于脂质过氧化物的产生、细胞膜损伤，最终导致细胞死亡。因此，引发铁死亡的信号通路与保护细胞免受铁过量和/或脂质衍生的活性氧影响的信号通路密切相关。在此，我们讨论铁死亡代谢途径与抗氧化系统之间的相互作用，特别关注参与铁死亡调节的转录因子，这些转录因子既可以作为脂质过氧化的触发因素，也可以作为铁死亡抗氧化防御途径。
