Glycophagy: An emerging target in pathology.

Autophagy, a highly conserved self-digestion process, is initially regarded as non-selectively sequestering and degradation cytoplasmic contents. Nowadays, many kinds of selective autophagy have been found in response to various physiological cues such as mitophagy, reticulophagy and glycophagy. Glycophagy, as a selective autophagy, plays a crucial role in maintaining glucose homeostasis in many tissues including heart, liver and skeletal muscles. Moreover, glycophagy is highly regulated by many signal pathways like the cyclic AMP protein kinase A/protein kinase A, PI3K-Akt/PKB-mTOR and Calcium. Latest studies have demonstrated that glycophagy is triggered by STBD1, which tethers glycogen to membranes via binding itself to the cognate autophagy protein GABARAPL1. More importantly, glycophagy might act as a protective role in coping with the accumulation of glycogen-rich lysosomes in infant patients with Pompe disease. However, glycophagy might aggravate diabetic cardiomyopathy via FoxO1 signal pathway. In this review, we focus on some findings about the occurrence and development, as well as the regulatory mechanism of glycophagy. We also analyze the role of glycophagy in Pompe disease and diabetic cardiomyopathy. Targeting glycophagy may open a new avenue of therapeutic intervention to these diseases.