CALCOCO1, also known as calcium binding and coiled-coil domain 1, is an important autophagy receptor. It is involved in the autophagic degradation of specific organelles, playing a crucial role in maintaining cellular homeostasis. It participates in pathways such as reticulophagy (endoplasmic reticulum selective autophagy) and Golgiphagy (autophagic degradation of the Golgi) [1,2,3,4,5].

Depletion of CALCOCO1 in cultured cells led to impaired ER degradation during stress, causing expansion of the ER and inefficient basal autophagy flux, suggesting its key role in maintaining ER homeostasis [3,4]. In the context of Golgi, lack of CALCOCO1 in cells causes an impaired Golgiphagy and expansion of the Golgi, indicating its importance in Golgi turnover [1,5].

In conclusion, CALCOCO1 is essential for maintaining the integrity and proper function of the endoplasmic reticulum and Golgi through its role in reticulophagy and Golgiphagy. Studies involving CALCOCO1-depleted cells have revealed its significance in these organellar homeostatic processes, providing insights into potential mechanisms underlying diseases related to organellar dysfunction.