Mitochondrial autophagy (mitophagy) is the selective clearance of damaged or incomplete mitochondria by autophagy, which is critical for the functional integrity of the entire mitochondrial network and cell survival. Because dysfunction of mitophagy is closely related to many diseases, it is important to study the specific molecular mechanism and pathophysiological significance of mitophagy. FUN14 domain-containing 1 (FUNDC1) is a newly identified mitochondrial outer membrane protein that induces receptor-mediated mitophagy by its interaction with LC3 during hypoxia. The expression, phosphorylation, regulation and significance of FUNDC1 are reviewed in the context of a large number of pathophysiological conditions. Emerging evidence has demonstrated that levels and phosphorylation states of FUNDC1 are closely related to occurrence, progression and prognosis of various diseases including heart diseases and cancers, indicating that FUNDC1 may serve as a promising biomarker and potential therapeutic target.

线粒体自噬（mitophagy）是通过自噬选择性清除受损或不完整的线粒体，这对于整个线粒体网络的功能完整性和细胞生存至关重要。由于线粒体自噬功能障碍与多种疾病密切相关，因此研究线粒体自噬的具体分子机制和病理生理意义具有重要意义。FUN14 结构域包含 1 (FUNDC1) 是一种新发现的线粒体外膜蛋白，在缺氧期间通过与 LC3 相互作用来诱导受体介导的线粒体自噬。在大量病理生理条件的背景下回顾了 FUNDC1 的表达、磷酸化、调控和意义。越来越多的证据表明，FUNDC1的水平和磷酸化状态与包括心脏病和癌症在内的多种疾病的发生、进展和预后密切相关，表明FUNDC1可能作为一种有前景的生物标志物和潜在的治疗靶点。