BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease.

BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease.
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BNIP3L/NIX 介导的线粒体自噬:分子机制及其对人类疾病的影响

DOI:
10.1038/s41419-021-04469-y
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发表时间:
2021-12-20
影响因子:
9
通讯作者:
Zhang X
Zhang X
中科院分区:
生物学1区
文献类型:
--
作者:
Li Y;Zheng W;Lu Y;Zheng Y;Pan L;Wu X;Yuan Y;Shen Z;Ma S;Zhang X;Wu J;Chen Z;Zhang X

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线粒体自噬是一种高度保守的细胞过程,通过自噬机制消除功能失调或多余的线粒体来维持线粒体数量。线粒体外膜蛋白BNIP3L/Nix通过识别自噬体作为线粒体自噬受体。最初已知BNIP3L在网状细胞发育过程中清除线粒体。最近的研究表明,它还参与多种生理和病理过程。本文综述了BNIP3L诱导有丝分裂的机制,并讨论了BNIP3L的生物学功能及其在分子水平上的调控。我们进一步讨论了bnip3l介导的线粒体自噬参与人类疾病,特别是癌症和神经系统疾病的现有证据。
Mitophagy is a highly conserved cellular process that maintains the mitochondrial quantity by eliminating dysfunctional or superfluous mitochondria through autophagy machinery. The mitochondrial outer membrane protein BNIP3L/Nix serves as a mitophagy receptor by recognizing autophagosomes. BNIP3L is initially known to clear the mitochondria during the development of reticulocytes. Recent studies indicated it also engages in a variety of physiological and pathological processes. In this review, we provide an overview of how BNIP3L induces mitophagy and discuss the biological functions of BNIP3L and its regulation at the molecular level. We further discuss current evidence indicating the involvement of BNIP3L-mediated mitophagy in human disease, particularly in cancer and neurological disorders.
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