Ferroptosis Is a Potential Therapeutic Target for Pulmonary Infectious Diseases

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology Pub Date : 2023-04-25 DOI:10.1155/2023/3875897

Yurong Zhang, Dianlun Qian, Xiangfeng Bai, Shibo Sun

引用次数: 0

Abstract

Ferroptosis is a new type of iron-dependent cell death caused by lipid peroxide (LPO) accumulation and involved in disease of pulmonary infection. The dysregulation of iron metabolism, the accumulation of LPO, and the inactivation and consumption of glutathione peroxidase 4 (GPX4) are the crucial cause of ferroptosis. Pulmonary infectious diseases caused by Pseudomonas aeruginosa (PA), Mycobacterium tuberculosis (MTB), and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) are associated with ferroptosis. Ferroptosis may be a potential therapeutic target for pulmonary infectious diseases. However, the mechanisms by which these infections are involved in ferroptosis and whether pulmonary infectious diseases caused by Staphylococcus aureus, Klebsiella pneumoniae, and Leishmania spp are related to ferroptosis are unclear. Accordingly, more researches are needed.

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铁下垂是肺部传染病的潜在治疗靶点

脱铁症是一种新型的由脂质过氧化物（LPO）积累引起的铁依赖性细胞死亡，与肺部感染有关。铁代谢的失调、LPO的积累以及谷胱甘肽过氧化物酶4（GPX4）的失活和消耗是脱铁症的关键原因。由铜绿假单胞菌（PA）、结核分枝杆菌（MTB）和严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）引起的肺部传染病与脱铁症有关。铁下垂可能是肺部感染性疾病的潜在治疗靶点。然而，这些感染与脱铁性贫血有关的机制以及由金黄色葡萄球菌、肺炎克雷伯菌和利什曼原虫引起的肺部感染性疾病是否与脱铁症有关尚不清楚。因此，还需要更多的研究。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.