Mitophagy and Ferroptosis in Sepsis-Induced ALI/ARDS: Molecular Mechanisms, Interactions and Therapeutic Prospects of Medicinal Plants.

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2024-10-29 eCollection Date: 2024-01-01 DOI:10.2147/JIR.S488655
Huixin Cheng, Xuehan Wang, Juyi Yao, Chunbo Yang, Jian Liu
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Abstract

Sepsis is a common critical illness characterized by high mortality rates and a significant disease burden. In the context of sepsis-induced organ dysfunction, the lungs are among the initial organs affected, which may progress to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Recent studies have highlighted the crucial roles of mitophagy and ferroptosis in the development and progression of sepsis-induced ALI/ARDS. Identifying key convergence points in these processes may provide valuable insights for the treatment of this condition. In recent years, certain herbs and their bioactive compounds have demonstrated unique benefits in managing sepsis-induced ALI/ARDS by modulating mitophagy or ferroptosis. This review summary the mechanisms of mitophagy and ferroptosis, explores their interactions, and emphasizes their regulatory roles in the progression of sepsis-induced ALI/ARDS. Additionally, it offers a novel perspective on treatment strategies by summarizing various herbs and their bioactive compounds relevant to this condition.

脓毒症诱发的 ALI/ARDS 中的有丝分裂和铁蛋白沉积:药用植物的分子机制、相互作用和治疗前景。
败血症是一种常见的危重病,其特点是死亡率高、疾病负担重。在脓毒症诱发的器官功能障碍中,肺是最初受影响的器官之一,可能发展为急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)。最近的研究强调了有丝分裂和铁蛋白沉积在脓毒症诱发的 ALI/ARDS 的发生和发展过程中的关键作用。确定这些过程中的关键汇合点可为治疗这种疾病提供有价值的见解。近年来,某些草药及其生物活性化合物通过调节有丝分裂或铁凋亡,在治疗脓毒症诱发的 ALI/ARDS 方面显示出独特的疗效。本综述总结了有丝分裂和铁突变的机制,探讨了它们之间的相互作用,并强调了它们在败血症诱发的 ALI/ARDS 进展过程中的调节作用。此外,它还总结了与该病症相关的各种草药及其生物活性化合物,为治疗策略提供了新的视角。
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
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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