有丝分裂在肺动脉高压中的作用：靶向机制与药物干预

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion Pub Date : 2024-07-09 DOI:10.1016/j.mito.2024.101928

Jia-Jing Wan , Jian Yi , Fei-Ying Wang , Xia Li , Chao Zhang , Lan Song , Ai-Guo Dai

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引用次数: 0

摘要

线粒体吞噬是真核细胞中的一个重要途径，它选择性地清除功能障碍的线粒体，从而通过线粒体质量控制维持细胞的平衡。肺动脉高压（PH）是指由于各种原因导致的肺动脉压力异常升高的一种病理状态，其潜在的发病机制至今仍难以捉摸。本文探讨了有丝分裂的分子机制，强调了它在 PH 中的作用以及在阐明相关分子信号通路方面取得的进展。此外，文章还重点介绍了目前的药物调控途径，旨在为肺动脉高压的预防和治疗提供新的见解。

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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Role of mitophagy in pulmonary hypertension: Targeting the mechanism and pharmacological intervention

Mitophagy, a crucial pathway in eukaryotic cells, selectively eliminates dysfunctional mitochondria, thereby maintaining cellular homeostasis via mitochondrial quality control. Pulmonary hypertension (PH) refers to a pathological condition where pulmonary arterial pressure is abnormally elevated due to various reasons, and the underlying pathogenesis remains elusive. This article examines the molecular mechanisms underlying mitophagy, emphasizing its role in PH and the progress in elucidating related molecular signaling pathways. Additionally, it highlights current drug regulatory pathways, aiming to provide novel insights into the prevention and treatment of pulmonary hypertension.

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来源期刊

Mitochondrion 生物-细胞生物学

CiteScore

9.40

自引率

4.50%

发文量

审稿时长

13.6 weeks

期刊介绍： Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.