Cell survival or death is one critical issue in inflammatory responses. Ferroptosis, which is characterized by iron-dependent lethal lipid peroxidation, has been found to participate in the development of cancers, degenerative brain diseases and ischemia-reperfusion injuries. Incorporation of polyunsaturated fatty acids (PUFAs) into cellular membranes represents a vulnerability to invasion of microbials and sterile stimuli. In addition, the competition for iron in the battle between microbials and host cells underlies infection development. Although host cells have been equipped with complex antioxidant systems to combat lethal accumulation of lipid peroxidation, emerging evidence suggests several pathogens may target PUFAs in the cell membrane, and manipulate ferroptosis as a way for pathogen propagation. Moreover, ferroptosis takes part in the progression of sterile inflammations, such as cigarette smoke-induced chronic obstructive pulmonary disease, stroke and ischemia-reperfusion injuries. As iron-dependent oxidative stress and lipid peroxidation are common features for ferroptosis and inflammatory diseases, underlying mechanisms linking such pathological conditions will be discussed in this review. Progress in the research of ferroptosis may shed more light on the etiology and treatment of inflammatory diseases.

细胞存活或死亡是炎症反应中的关键问题之一。现已发现以铁依赖性致死脂质过氧化作用为特征的Ferroptosis参与了癌症，变性脑疾病和局部缺血再灌注损伤的发展。将多不饱和脂肪酸（PUFA）掺入细胞膜代表了微生物入侵和无菌刺激的脆弱性。另外，微生物与宿主细胞之间的竞争中铁的竞争是感染发展的基础。尽管宿主细胞已经配备了复杂的抗氧化剂系统来对抗脂质过氧化的致命积累，但新兴证据表明，多种病原体可能靶向细胞膜中的PUFA，并操纵肥大病作为病原体繁殖的一种方式。此外，肥大症参与无菌性炎症的发展，例如香烟烟雾引起的慢性阻塞性肺疾病，中风和缺血再灌注损伤。由于铁依赖性氧化应激和脂质过氧化作用是肥大症和炎症性疾病的共同特征，因此在本综述中将讨论与这种病理状况相关的潜在机制。铁症病的研究进展可能会为炎症性疾病的病因和治疗提供更多的启示。在这篇综述中将讨论与这种病理状况相关的潜在机制。铁症病的研究进展可能会为炎症性疾病的病因和治疗提供更多的启示。在这篇综述中将讨论与这种病理状况相关的潜在机制。铁症病的研究进展可能会为炎症性疾病的病因和治疗提供更多的启示。