Ccpg1, also known as cell cycle progression 1, is a non-canonical autophagy cargo receptor. It is essential for reticulophagy (the selective autophagy of the endoplasmic reticulum, ER-phagy), which plays a crucial role in maintaining ER proteostasis. Ccpg1 can bind to Atg8-family proteins and RB1CC1/FIP200, facilitating its function as a cargo receptor. The plasticity of autophagy, in which Ccpg1 is involved, has implications for understanding cellular metabolism and homeostasis [2,3,4,5].

In a study on corneal Aspergillus fumigatus infection, the expression of Ccpg1 in human corneal epithelial cells (HCECs) and human myeloid leukemia mononuclear cells (THP-1) macrophages increased in a time-dependent manner after infection. Its up-regulation in response to the infection was independent of dectin-1, and it colocalized with C-type lectin-like receptor-1 (CLEC-1) in THP-1 macrophages, indicating its involvement in the corneal antifungal immune response [1]. In pancreatic acinar cells, in vivo studies have shown that Ccpg1 prevents the hyper-accumulation of insoluble protein within the ER lumen, alleviates ER stress, and its loss sensitizes the exocrine pancreas to tissue injury. Ccpg1 transcripts are inducible by ER stress, directly linking ER stress to reticulophagy [4,5].

In conclusion, Ccpg1 is vital for maintaining ER proteostasis through its role in reticulophagy. Its function has been demonstrated in both corneal antifungal immune response and pancreatic ER stress management. The in vivo studies, especially those using models where Ccpg1 function is disrupted, have provided valuable insights into its role in these specific biological processes and potential implications for related disease conditions.