Autophagy, an evolutionarily conserved process for maintaining the physio‐metabolic equilibrium of cells, shares many common effector proteins with endocytosis. For example, tethering proteins involved in fusion like Ras‐like GTPases (Rabs), soluble N‐ethylmaleimide sensitive factor attachment protein receptors (SNAREs), lysosomal‐associated membrane protein (LAMP), and endosomal sorting complex required for transport (ESCRT) have a dual role in endocytosis and autophagy, and the trafficking routes of these processes converge at lysosomes. These common effectors indicate an association between budding and fusion of membrane‐bound vesicles that may have a substantial role in autophagic lysosome reformation, by sensing cellular stress levels. Therefore, autophagy–endocytosis crosstalk may be significant and implicates a novel endocytic regulatory pathway of autophagy. Moreover, endocytosis has a pivotal role in the intake of signalling molecules, which in turn activates cascades that can result in pathophysiological conditions. This review discusses the basic mechanisms of this crosstalk and its implications in order to identify potential novel therapeutic targets for various human diseases.

中文翻译：

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自噬和内吞作用在人类健康和疾病中的分子相互作用

自噬是一种维持细胞生理代谢平衡的进化保守过程，与内吞作用共享许多常见的效应蛋白。例如，参与融合的束缚蛋白如 Ras 样 GTPases (Rabs)、可溶性 N-乙基马来酰亚胺敏感因子附着蛋白受体 (SNAREs)、溶酶体相关膜蛋白 (LAMP) 和转运所需的内体分选复合体 (ESCRT)在内吞作用和自噬中具有双重作用，这些过程的运输途径会聚在溶酶体上。这些常见的效应子表明膜结合囊泡的出芽和融合之间存在关联，通过感知细胞应激水平，膜结合囊泡可能在自噬溶酶体重组中起重要作用。所以，自噬-内吞作用串扰可能很重要，并暗示了一种新的自噬内吞调节途径。此外，内吞作用在信号分子的摄入中起关键作用，信号分子反过来激活可能导致病理生理状况的级联反应。本综述讨论了这种串扰的基本机制及其影响，以确定各种人类疾病的潜在新治疗靶点。