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

Med Sci Monit. 2020 Sep 10:26:e924558. doi: 10.12659/MSM.924558.

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.

Publication types

  • Review

MeSH terms

  • Apoptosis / drug effects*
  • Autophagy / drug effects*
  • Cardiovascular Diseases* / drug therapy
  • Cardiovascular Diseases* / metabolism
  • Cardiovascular Diseases* / pathology
  • Catechin / analogs & derivatives*
  • Catechin / therapeutic use
  • Diabetes Mellitus* / drug therapy
  • Diabetes Mellitus* / metabolism
  • Diabetes Mellitus* / pathology
  • Endoplasmic Reticulum Chaperone BiP
  • Endoplasmic Reticulum Stress / drug effects*
  • Humans
  • Neoplasms* / drug therapy
  • Neoplasms* / metabolism
  • Neoplasms* / pathology
  • Nervous System Diseases* / drug therapy
  • Nervous System Diseases* / metabolism
  • Nervous System Diseases* / pathology
  • Signal Transduction / drug effects*

Substances

  • Endoplasmic Reticulum Chaperone BiP
  • HSPA5 protein, human
  • Catechin
  • epigallocatechin gallate