Abstract：
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.
摘要：
线粒体自噬,真核细胞中的关键途径，选择性地消除功能失调的线粒体，从而通过线粒体质量控制维持细胞稳态。肺动脉高压（PH）是指由于各种原因导致肺动脉压异常升高的病理状况。潜在的发病机制仍然难以捉摸。本文研究了线粒体自噬的分子机制，强调其在PH中的作用以及阐明相关分子信号通路的进展。此外,它突出了当前的药物监管途径，旨在为肺动脉高压的预防和治疗提供新的见解。
