A Review of Traditional Chinese Medicine in Treating Renal Interstitial Fibrosis via Endoplasmic Reticulum Stress-Mediated Apoptosis

Figure 1

Mechanisms of ER stress-mediated apoptosis. Once PERK is activated, eIF2α is phosphorylated to achieve ATF4 translation and CHOP activation. Activation of the IRE1α domain processes uncut XBP1mRNA to produce activated XBP1(s), which enters the nucleus and controls the expression of CHOP. ATF6α is transported to the Golgi apparatus, where it is processed by the proteases SP1 and SP2 to produce cytoplasmic fragment ATF6, which regulates CHOP activation in the nucleus. CHOP can trigger the endogenous apoptosis pathway and promote cell apoptosis by inhibiting the upregulation of BCL-2. CHOP can also upregulate the expression of TRB3, preventing Akt phosphorylation. CHOP can also initiate the exogenous apoptosis pathway through DR4 and DR5 and can additionally trigger the ERO1α-IP3R-Ca²⁺-CaMKII pathway.