PDF(Pubmed)
Abstract：
Mitophagy is a cellular process that enables the selective degradation of damaged, dysfunctional, or superfluous mitochondria. During mitophagy, specific proteins recognize and tag mitochondria for degradation. These tagged mitochondria are engulfed by specialized structures called phagophores that then mature into autophagosomes/mitophagosomes. Mitophagosomes subsequently transport their mitochondrial cargo to lysosomes, where the mitochondria are broken down and recycled. While the PINK1-PRKN-dependent mitophagy pathway is well understood, mitophagy can also occur independently of this pathway. BNIP3 and BNIP3L/NIX, paralogous membrane proteins on the outer mitochondrial membrane (OMM), serve as ubiquitin-independent mitophagy receptors. Historically, BNIP3 regulation was thought to be primarily transcriptional through HIF1A (hypoxia inducible factor 1 subunit alpha). However, recent work has revealed a significant post-translational dimension, highlighting the strong role of the ubiquitin-proteasome system (UPS) in BNIP3 regulation. With these emerging concepts in mind, we aimed to develop a unified understanding of how steady-state levels of BNIP3 are established and maintained and how this regulation governs underlying cell physiology.
摘要：
线粒体自噬是一种细胞过程，能够选择性地降解受损的细胞，功能失调,或者多余的线粒体.在线粒体自噬期间，特定的蛋白质识别和标记线粒体降解。这些标记的线粒体被称为吞噬细胞的专门结构吞噬，然后成熟为自噬体/线粒体吞噬体。线粒体吞噬体随后将其线粒体货物运输到溶酶体，线粒体被分解和回收。虽然PINK1-PRKN依赖性线粒体自噬途径是众所周知的，线粒体自噬也可以独立于该途径发生。BNIP3和BNIP3L/NIX,线粒体外膜（OMM）上的旁系膜蛋白，作为泛素非依赖性线粒体自噬受体。历史上,BNIP3调节被认为主要通过HIF1A(缺氧诱导因子1亚基α)转录。然而,最近的工作揭示了一个重要的翻译后维度，强调泛素-蛋白酶体系统（UPS）在BNIP3调节中的重要作用。考虑到这些新兴的概念，我们的目的是对如何建立和维持BNIP3的稳态水平以及该调节如何控制潜在的细胞生理学进行统一的理解.
