各种肺部疾病中与铁下垂相关的分子机制以及肺癌可能的治疗方案。

Doaa Ghareeb, Maysara El-Salakawy
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摘要

细胞死亡是一个自然过程,在这个过程中,旧的或不需要的细胞被破坏,并被一个新的功能细胞所取代。多种因素触发细胞死亡,并存在多种机制,如细胞凋亡、自噬和铁下垂。铁死亡是一种新型的程序性细胞死亡,是由于细胞铁积累和细胞抗氧化酶之一谷胱甘肽过氧化物酶4 (GPX-4)的消耗而发生的。因此,铁下垂以脂质过氧化和氧化应激为特征。铁、氨基酸、脂质代谢等代谢途径被认为是铁下垂过程的调节因子。一些研究已经证明,从急性肺损伤(ALI)到慢性肺损伤,铁下垂与肺部疾病的进展/抑郁有关
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Molecular mechanisms associated with ferroptosis during various pulmonary disorders and the possible therapeutic regimens for lung cancer.
: Cell death is the natural process in which the old or unwanted cell is damaged and replaced by a newly functional one. Several factors trigger cell death and there are several mechanisms for this event such as apoptosis, autophagy, and ferroptosis. Ferroptosis as a novel type of programmed cell death is occurred due to cellular iron accumulation and the depletion in one of cellular antioxidant enzymes which is glutathione peroxidase 4 (GPX-4). Therefore, ferroptosis is characterized by lipid peroxidation and oxidative stress. Several metabolic pathways such as iron, amino acids, lipids metabolism, etc are considered as regulators for ferroptosis process. Several studies have proved the involvement of ferroptosis in lung diseases progression/depression that range from acute lung injury (ALI) to
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