Cullin-RING ligases (CRLs), the largest E3 ubiquitin ligase family, promote ubiquitination and degradation of various cellular key regulators involved in a broad array of physiological and pathological processes, including cell cycle progression, signal transduction, transcription, cardiomyopathy, and tumorigenesis. Autophagy, an intracellular catabolic reaction that delivers cytoplasmic components to lysosomes for degradation, is crucial for cellular metabolism and homeostasis. The dysfunction of autophagy has been proved to associate with a variety of human diseases. Recent evidences revealed the emerging roles of CRLs in the regulation of autophagy. In this review, we will focus mainly on recent advances in our understandings of the regulation of autophagy by CRLs and the cross-talk between CRLs and autophagy, two degradation systems. We will also discuss the pathogenesis of human diseases associated with the dysregulation of CRLs and autophagy. Finally, we will discuss current efforts and future perspectives on basic and translational research on CRLs and autophagy.

中文翻译：

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Cullin-RING连接酶可调节自噬。

Cullin-ring连接酶（CRL）是最大的E3泛素连接酶家族，可促进涉及广泛的生理和病理过程的各种细胞关键调节剂的泛素化和降解，包括细胞周期进程，信号转导，转录，心肌病和肿瘤发生。自噬是一种细胞内分解代谢反应，可将细胞质成分传递至溶酶体进行降解，对于细胞代谢和体内平衡至关重要。自噬功能障碍已被证明与多种人类疾病有关。最近的证据揭示了CRL在自噬调节中的新兴作用。在这篇综述中，我们将主要关注我们对CRLs自噬调控以及CRL和自噬这两个降解系统之间的相互影响的理解的最新进展。我们还将讨论与CRLs和自噬失调有关的人类疾病的发病机理。最后，我们将讨论有关CRL和自噬的基础和转化研究的当前努力和未来展望。