The present review is a summary of the recent literature concerning Bnip3 expression, function, and regulation, along with its implications in mitochondrial dysfunction, disorders of mitophagy homeostasis, and development of diseases of secondary mitochondrial dysfunction. As a member of the Bcl-2 family of cell death-regulating factors, Bnip3 mediates mPTP opening, mitochondrial potential, oxidative stress, calcium overload, mitochondrial respiratory collapse, and ATP shortage of mitochondria from multiple cells. Recent studies have discovered that Bnip3 regulates mitochondrial dysfunction, mitochondrial fragmentation, mitophagy, cell apoptosis, and the development of lipid disorder diseases via numerous cellular signaling pathways. In addition, Bnip3 promotes the development of cardiac hypertrophy by mediating inflammatory response or the related signaling pathways of cardiomyocytes and is also responsible for raising abnormal mitophagy and apoptosis progression through multiple molecular signaling pathways, inducing the pathogenesis and progress of hepatocellular carcinoma (HCC). Different molecules regulate Bnip3 expression at both the transcriptional and post-transcriptional level, leading to mitochondrial dysfunction and unbalance of mitophagy in hepatocytes, which promotes the development of non-alcoholic fatty liver disease (NAFLD). Thus, Bnip3 plays an important role in mitochondrial dysfunction and mitophagy homeostasis and has emerged as a promising therapeutic target for diseases of secondary mitochondrial dysfunction.

中文翻译：

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线粒体中的Bnip3：继发性线粒体功能障碍疾病的新见解和潜在治疗靶标。

本文综述了有关Bnip3表达，功能和调控的最新文献，以及其对线粒体功能障碍，线粒体稳态障碍和继发性线粒体功能障碍疾病发展的影响。作为Bcl-2细胞死亡调节因子家族的成员，Bnip3介导了mPTP的开放，线粒体电位，氧化应激，钙超载，线粒体呼吸衰竭和多细胞线粒体的ATP缺乏。最近的研究发现，Bnip3通过许多细胞信号途径调节线粒体功能障碍，线粒体片段化，线粒体，细胞凋亡以及脂质疾病的发展。此外，Bnip3通过介导炎症反应或心肌细胞的相关信号通路来促进心脏肥大的发展，并且还负责通过多种分子信号通路提高异常线粒体和细胞凋亡的进程，诱导肝细胞癌（HCC）的发病机理和进展。不同的分子在转录水平和转录后水平均调节Bnip3的表达，从而导致肝细胞线粒体功能障碍和线粒体不平衡，从而促进了非酒精性脂肪性肝病（NAFLD）的发展。因此，Bnip3在线粒体功能障碍和线粒体稳态中发挥重要作用，并已成为继发性线粒体功能障碍疾病的有希望的治疗靶标。