The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseases

Abstract

Tea containing abundant catechins is a popular non-alcoholic beverage worldwide. Epigallocatechin-3-gallate (EGCG) is the predominately active substance in catechins, exhibiting a wide range of functional properties including cancer suppression, neuroprotective, metabolic regulation, cardiovascular protection, stress adjustment, and antioxidant in various diseases. Autophagy, a basic cell function, participates in various physiological processes which include clearing away abnormally folded proteins and damaged organelles, and regulating growth. EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation, but also causing LC3 transition and decreasing p62 expression. EGCG-induced autophagy is involved in the occurrence and development of many human diseases, including cancer, neurological diseases, diabetes, cardiovascular diseases, and injury. Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS) as a cellular stress response which is caused by various internal and external factors. ERS-induced apoptosis of EGCG influences cell survival and death in various diseases via regulating IRE1, ATF6, and PERK signaling pathways, and activating GRP78 and caspase proteins. The present manuscript reviews that the effect of EGCG in autophagy and ERS-induced apoptosis of human diseases.

Figure 1

Mechanism of EGCG in autophagy and ERS-induced apoptosis in human disease. EGCG – epigallocatechin-3-gallate; ERS – endoplasmic reticulum stress; ROS – reactive oxygen species.