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环境污染物诱导的铁死亡在肺部疾病中的作用。

Role of environmental pollutants-induced ferroptosis in pulmonary diseases.

作者信息

Yang Long, Qiao Yongkang, Huang Zeyu, Chen Yuzhu, Zhang Enxi, Liu Zhiwei, Wang Yuxuan, Chen Shaobo, Dong Jinrui, Liu Bin

机构信息

Integrated Medical Center, Tianjin University, Tianjin, China.

Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, Beijing Normal University, Zhuhai, Guangdong, China.

出版信息

Front Med (Lausanne). 2025 Feb 24;12:1542275. doi: 10.3389/fmed.2025.1542275. eCollection 2025.

Abstract

Respiratory diseases rank among the foremost causes of mortality and disability globally, with long-term exposure to environmental pollutants playing a critical role in their onset and progression. Despite this, the underlying mechanisms and effective targeted treatments for these disorders remain poorly understood, highlighting an urgent need for focused research. Cell death, a programmed cellular response to external harmful stimuli, including ferroptosis-a recently identified form of iron-dependent programmed cell death-emerges as a pivotal process. Characterized by intracellular iron accumulation and lipid peroxidation, ferroptosis appears intricately linked to lung injury induced by environmental pollutants. This review examines the role of ferroptosis in lung diseases triggered by environmental factors, aiming to shed light on its specific pathophysiological mechanisms and potential as a therapeutic target. By deepening our understanding of the interactions between environmental pollution, ferroptosis, and lung damage, we hope to inform strategies for effective intervention.

摘要

呼吸系统疾病是全球死亡和残疾的主要原因之一,长期暴露于环境污染物在其发病和进展中起着关键作用。尽管如此,这些疾病的潜在机制和有效的靶向治疗方法仍知之甚少,这凸显了开展针对性研究的迫切需求。细胞死亡是细胞对外部有害刺激的一种程序性反应,包括铁死亡(一种最近发现的铁依赖性程序性细胞死亡形式),它已成为一个关键过程。铁死亡的特征是细胞内铁积累和脂质过氧化,它似乎与环境污染物引起的肺损伤有着复杂的联系。这篇综述探讨了铁死亡在环境因素引发的肺部疾病中的作用,旨在阐明其具体的病理生理机制以及作为治疗靶点的潜力。通过加深我们对环境污染、铁死亡和肺损伤之间相互作用的理解,我们希望为有效的干预策略提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd7b/11891068/2b54b92d7f66/fmed-12-1542275-g001.jpg

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